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24.1: Introduction to Digestive System Processes and Regulation - Biology

24.1: Introduction to Digestive System Processes and Regulation - Biology


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Discuss the processes and regulations involved in digestion

Obtaining nutrition and energy from food is a multi-step process. The functions of the digestive system are regulated through neural and hormonal responses.

What You’ll Learn to Do

  • Detail the steps involved in the digestive system processes
  • Discuss the role of neural regulation in digestive processes
  • Explain how hormones regulate digestion

Learning Activities

The learning activities for this section include the following:

  • Digestive System Processes
  • Neural Responses to Food
  • Hormonal Responses to Food
  • Self Check: Digestive System Regulation

24.3 Lipid Metabolism

Fats (or triglycerides) within the body are ingested as food or synthesized by adipocytes or hepatocytes from carbohydrate precursors (Figure 24.3.1). Lipid metabolism entails the oxidation of fatty acids to either generate energy or synthesize new lipids from smaller constituent molecules. Lipid metabolism is associated with carbohydrate metabolism, as products of glucose (such as acetyl CoA) can be converted into lipids.

Figure 24.3.1 – Triglyceride Broken Down into a Monoglyceride: A triglyceride molecule (a) breaks down into a monoglyceride and two free fatty acids (b).

Lipid metabolism begins in the intestine where ingested triglycerides are broken down into free fatty acids and a monoglyceride molecule (see Figure 24.3.1b) by pancreatic lipases, enzymes that break down fats after they are emulsified by bile salts. When food reaches the small intestine in the form of chyme, a digestive hormone called cholecystokinin (CCK) is released by intestinal cells in the intestinal mucosa. CCK stimulates the release of pancreatic lipase from the pancreas and stimulates the contraction of the gallbladder to release stored bile salts into the intestine. CCK also travels to the brain, where it can act as a hunger suppressant.

Once the bile salts have emulsified the triglycerides, the pancreatic lipases down triglycerides into free fatty acids. These fatty acids can be transported across the intestinal membrane. However, once they cross the membrane, they are recombined to again form triglyceride molecules. Within the intestinal cells, these triglycerides are packaged along with cholesterol molecules in phospholipid vesicles called chylomicrons (Figure 24.3.2). The chylomicrons enable fats and cholesterol to move within the aqueous environment of your lymphatic and circulatory systems. Chylomicrons leave the enterocytes by exocytosis and enter the lymphatic system via lacteals in the villi of the intestine. From the lymphatic system, the chylomicrons are transported to the circulatory system. Once in the circulation, they can either go to the liver or be stored in fat cells (adipocytes) that comprise adipose (fat) tissue found throughout the body.

Figure 24.3.2 – Chylomicrons: Chylomicrons contain triglycerides, cholesterol molecules, and other apolipoproteins (protein molecules). They function to carry these water-insoluble molecules from the intestine, through the lymphatic system, and into the bloodstream, which carries the lipids to adipose tissue for storage.


Carbohydrates

The digestion of carbohydrates begins in the mouth. The salivary enzyme amylase begins the breakdown of food starches into maltose, a disaccharide. As the bolus of food travels through the esophagus to the stomach, no significant digestion of carbohydrates takes place. The esophagus produces no digestive enzymes but does produce mucous for lubrication. The acidic environment in the stomach stops the action of the amylase enzyme.

The next step of carbohydrate digestion takes place in the duodenum. Recall that the chyme from the stomach enters the duodenum and mixes with the digestive secretion from the pancreas, liver, and gallbladder. Pancreatic juices also contain amylase, which continues the breakdown of starch and glycogen into maltose, a disaccharide. The disaccharides are broken down into monosaccharides by enzymes called maltases

, sucrases, and lactases, which are also present in the brush border of the small intestinal wall. Maltase breaks down maltose into glucose. Other disaccharides, such as sucrose and lactose are broken down by sucrase and lactase, respectively. Sucrase breaks down sucrose (or “table sugar”) into glucose and fructose, and lactase breaks down lactose (or “milk sugar”) into glucose and galactose. The monosaccharides (glucose) thus produced are absorbed and then can be used in metabolic pathways to harness energy. The monosaccharides are transported across the intestinal epithelium into the bloodstream to be transported to the different cells in the body. The steps in carbohydrate digestion are summarized in Figure 15.16 and Table 15.5.

Figure 15.16. Digestion of carbohydrates is performed by several enzymes. Starch and glycogen are broken down into glucose by amylase and maltase. Sucrose (table sugar) and lactose (milk sugar) are broken down by sucrase and lactase, respectively.

Table15 .5 Digestion of Carbohydrates
Enzyme Produced By Site of Action Substrate Acting On End Products
Salivary amylase Salivary glands Mouth Polysaccharides (Starch) Disaccharides (maltose), oligosaccharides
Pancreatic amylase Pancreas Small intestine Polysaccharides (starch) Disaccharides (maltose), monosaccharides
Oligosaccharidases Lining of the intestine brush border membrane Small intestine Disaccharides Monosaccharides (e.g., glucose, fructose, galactose)

Materials and methods

Animals and their maintenance

The five species of this study span the geographic range and morphological diversity of the genus Python(Fig. 1). Python brongersmai Stull 1938, the blood python, inhabits eastern Sumatra and neighboring portions of Malaysia (Keogh et al., 2001). They are an extremely heavy-bodied snake [body mass to total length ratio of 8.97±0.23 (mean ± 1 s.e.m.) Fig. 1] with a body mass reaching 22 kg and a body length up to 2.5 m(Shine et al., 1999 Keogh et al., 2001). Python molurus L. is a large snake, up to 8 m in length and 100 kg in mass that ranges from India east into Thailand(Murphy and Henderson, 1997). Python regius Shaw 1802, the ball python, inhabits west-central Africa and is the smallest of the Python species (2 m) and is stout in body shape (Obst et al.,1984). Python reticulatus Schneider 1801, the reticulated python, ranges throughout southeastern Asia and Indonesia(Pope, 1961). Considered the longest snake in the world (reported lengths of 10 m), P. reticulatushas the most slender body shape (body mass to total length ratio of 4.53±0.18 Fig. 1) of the Python species used in this study. Python sebae Gmelin 1789, the northern African python, occurs throughout much of the northern portion of sub-Saharan Africa and is also a large python (8 m in length and 100 kg in mass) with a body shape similar to that of P. molurus(Broadley, 1984). In general, Python species are considered to be sit-and-wait foragers that feed relatively infrequently in the wild (Pope,1961 Murphy and Henderson,1997). Sit-and-wait foraging snakes lie in wait in a camouflaged location from which they can ambush passing prey(Pope, 1961 Slip and Shine, 1988 Greene, 1997).

The pythons used in this study were born in captivity and purchased commercially. We housed snakes individually in 20 l plastic boxes and maintained them at 28-32°C under a photoperiod of 14 h:10 h L:D. Snakes were fed laboratory rats once every 2 weeks and had continuous access to water. To reduce potential body-size effects, we used snakes of similar mass resulting in no significant difference among the five Python species in body mass for either the metabolic or intestinal experiments. Prior to the start of experimentation, we withheld food from snakes for a minimum of 30 days to ensure that they were postabsorptive. Python molurus has been found to complete digestion within 10-14 days after feeding(Secor and Diamond, 1995). All individual snakes used in this study were between 18 and 24 months old, with body masses of studied P. brongersmai, P. molurus, P. regius, P. reticulatus and P. sebae averaging 806±51 (N=9),760±47 (N=7), 707±71 (N=10), 757±49(N=10) and 759±47 (N=10) g, respectively. Animal care and experimentation were conducted under protocols approved by the University of Alabama Institutional Animal Care and Use Committee.

Photographs and relative body shape (body mass, Mb/total length, TL) of the five Pythonspecies used in this study. (A) P. brongersmai, (B) P. regius, (C) P. sebae, (D) P. molurus, (E) P. reticulatus. Note the significant variation in body shape from the short and stout P. brongersmai to the long and slender P. reticulatus. In the histogram, letters above bars that are different denote significant (P<0.05) differences between means, as determined from post hoc pairwise comparisons.

Photographs and relative body shape (body mass, Mb/total length, TL) of the five Pythonspecies used in this study. (A) P. brongersmai, (B) P. regius, (C) P. sebae, (D) P. molurus, (E) P. reticulatus. Note the significant variation in body shape from the short and stout P. brongersmai to the long and slender P. reticulatus. In the histogram, letters above bars that are different denote significant (P<0.05) differences between means, as determined from post hoc pairwise comparisons.

Measurements of postprandial metabolic response

We quantified the postprandial metabolic response of each species by measuring rates of oxygen consumption(O2) from snakes fasted for 30 days and following feeding. Measurements were made using closed-system respirometry as described(Secor and Diamond, 1997 Secor, 2003). Each metabolic trial began by measuring O2 of fasted snakes twice a day (morning and evening) for up to 6 days and assigning the lowest measured O2 of each snake over that time period as its standard metabolic rate (SMR). Snakes were then fed a meal consisting of one to three rats equaling 25.0±0.0% of their body mass and metabolic measurements were resumed at 12-h intervals for 3 days and at 24-h intervals thereafter for 11 more days. At 5-day intervals during metabolic measurements, snakes were removed from their chambers, weighed,provided with water, and then returned back to their chambers.

We characterized the postprandial metabolic response of meal break down,absorption and assimilation of each snake by quantifying the following six variables as described by Secor and Faulkner(Secor and Faulkner, 2002):(1) SMR, the lowest measured O2 prior to feeding (2) peak O2, the highest recorded O2following feeding (3) factorial scope of peak O2, calculated as peak O2divided by SMR (4) duration, the time after feeding that O2 was significantly elevated above SMR (5) SDA, specific dynamic action: the total energy expenditure above SMR over the duration of significantly elevated O2 and (6) SDA coefficient, SDA quantified as a percentage of meal energy. We quantified SDA(kJ) by summing the extra O2 consumed above SMR during the period of significantly elevated O2 and multiplying that value by 19.8 J ml -1 O2 consumed assuming that the dry matter of the catabolized rodent meal is 70% protein,25% fat and 5% carbohydrates, and generates a respiratory quotient (RQ) of 0.73 (Gessaman and Nagy, 1988). The energy content of rodent meals was calculated by multiplying the rodent wet mass by its energy equivalent (kJ g -1 wet mass) determined by bomb calorimetry. Five individual rats,each of three different size classes, were weighed (wet mass), dried,reweighed (dry mass), ground to a fine powder, and pressed into pellets. Three pellets from each individual rat were ignited in a bomb calorimeter (1266,Parr Instruments Co., Moline, IL, USA) to determine energy content (kJ g -1 ). For each rat, we determined wet-mass energy equivalent as the product of dry mass energy content and rodent's dry mass percentage. The three rodent size classes we used weighed on average 45±0.2, 65±5.0 and 150±5.0 g and had an energy equivalent of 6.5±0.3,7.0±0.4 and 7.6±0.3 kJ g -1 wet mass,respectively.

Tissue collection

For each species, we killed (by severing the spinal cord immediately posterior to the head) three individuals that had been fasted for 30 days and three individuals 2 days following the consumption of rodent meals equaling 25% of the snake's body mass. Following death, a mid-ventral incision was made to expose the GI tract and other internal organs, which were each removed and weighed. We emptied the contents of the stomach, small intestine and large intestine of fed snakes and reweighed each organ. The difference between full and empty weight of each organ was noted as the mass of the organ's content. Organ content mass was divided by meal mass to illustrate for each species the relative extent of digestion at 2 days postfeeding.

Intestinal nutrient uptake

In fasted and digesting snakes we measured nutrient transport rates across the intestinal brush border membrane using the everted sleeve technique as developed by Karasov and Diamond (Karasov and Diamond, 1983) and modified for snakes by Secor et al.(Secor et al., 1994) and Secor and Diamond (Secor and Diamond,2000). The empty small intestine was everted (turned inside out),divided into equal-length thirds each third was weighed and sectioned into 1-cm segments. Segments were mounted on metal rods, preincubated in reptile Ringer's solution at 30°C for 5 min, and then incubated for 2 min at 30°C in reptile Ringer's solution containing an unlabeled and radiolabeled nutrient and a radiolabeled adherent fluid marker ( l -glucose or polyethylene glycol). We measured, from individual intestinal segments, total uptake (passive and carrier-mediated) of the amino acids l -leucine and l -proline and active carrier-mediated uptake of d -glucose. Because of the similarities between uptake rates of the proximal and middle intestinal regions, we report the average uptake rates of those two segments (noted hereafter as the anterior intestine) and those of the distal segment.

A pair of studies has shown the everted sleeve technique to severely damage the intestinal mucosa of birds, and thus question the method's ability to accurately quantify intestinal performance for those species (Starck et al.,2000 Stein and Williams,2003). To determine whether the method has any damaging effects on python intestine, we compared sets of intestinal segments removed from the proximal region of the small intestine of fed P. molurus, P. reticulatus and P. sebae at two stages of the everted sleeve protocol prior to eversion and after everted tissues were incubated at 30°C in unstirred reptile Ringers for 5 min and in stirred reptile Ringers for 2 min. We prepared each intestinal segment for light microscopy (described below) and examined cross sections of the intestine for damage to the mucosal layer.

For each of these three pythons, everting, mounting and incubating intestinal segments did not damage the mucosal layer. Between the two stages of the procedure, we observed no significant difference (all P>0.47) in villus length (N=20 per stage of procedure)for these three species. In contrast to some birds, the everted sleeve can be performed without damaging the intestinal mucosa of pythons, as well as the mucosa of lizards and anurans (Secor,2005b Tracy and Diamond,2005).

Brush border enzyme activity

From each intestinal third we measured the activity of the brush border-bound hydrolase, aminopeptidase-N (EC 3.4.11.2) following the procedure of Wojnarowska and Gray (Wojnarowska and Gray, 1975). Aminopeptidase-N cleaves NH2-terminal amino acid residues from luminal oligopeptides to produce dipeptides and amino acids that then can be absorbed by the small intestine(Ahnen et al., 1982). From 1-cm segments, scraped mucosa was homogenized in PBS (1:250 dilutions) on ice. Activity of aminopeptidase-N was measured using leucyl-β-naphthylamide(LNA) as the substrate and p-hydroxymercuribenzoic acid to inhibit nonspecific cytosol peptidases. Absorbance of the product resulting from the hydrolysis of LNA was measured spectrophometrically (DU 530, Beckman Coulter,Inc., Fullerton, CA, USA) at 560 nm and compared to a standard curve developed with β-naphthylamine. Enzyme activities were quantified as μmol of substrate hydrolyzed per minute per gram of protein. Protein content of the homogenate was determined using the Bio-Rad Protein Assay kit based on the method of Bradford (Bradford,1976).

Intestinal morphology and organ masses

We quantified the effects of feeding on small intestinal morphology by measuring intestinal mass, intestinal length, mucosa and muscularis/serosa thickness and enterocyte dimensions from fasted and fed snakes. Immediately following the removal and flushing of the small intestine, we measured its wet mass and length. From the middle region of the small intestine, a 1-cm segment was fixed in 10% neutral-buffered formalin solution, embedded in paraffin and cross sectioned (6 μm). Several cross sections were placed on a glass slide and stained with Hematoxylin and Eosin. We measured mucosa and muscularis/serosa thickness and enterocyte dimensions from individual cross sections using a light microscope and video camera linked to a computer and image-analysis software (Motic Image Plus, Richmond, British Columbia,Canada). We calculated the average thickness of the mucosa and muscularis/serosa from ten measurements taken at different positions of the cross section. Likewise, we averaged the height and width of ten enterocytes measured at different positions of the cross section and calculated their volume based on the formula for a cube (enterocyte width 2 ×height). To assess postprandial effects on the mass of other organs, we weighed the wet mass of the heart, lungs, liver, empty stomach, pancreas,empty large intestine and kidneys immediately upon their removal from snakes. Each organ was dried at 60°C for 2 weeks and then reweighed for dry mass.

Small intestinal capacity

For each nutrient we quantified the intestine's total uptake capacity(reported as μmole min -1 ) by summing together the product of segment mass (mg) and mass-specific rates of nutrient uptake (nmole min -1 mg -1 ) for the proximal, middle and distal segments. Likewise, we quantified total small intestinal capacity for aminopeptidase-N activity by summing the products of mucosa segment mass (mg)times segment aminopeptidase-N activity, calculated as μmol of substrate hydrolyzed per minute per mg of mucosa. Mucosa mass was calculated from the mass of scraped mucosa from a 1-cm segment of intestine and multiplying that mass by segment length.

Statistical analyses

For each metabolic trial we used repeated-measures design analysis of variance (ANOVA) to test for significant effects of time (before and after feeding) on O2. Additionally, we used post hoc pairwise mean comparisons(Tukey-Kramer procedure) to determine when post feeding O2 was no longer significantly different from SMR, and to identify significant differences in O2 between sampling times. To test for species effects on metabolic variables, we used ANOVA for mass-specific rates and analysis of covariance (ANCOVA), with body mass as the covariate, for whole-animal measurements. Significant ANOVA and ANCOVA results were followed by post hoc comparisons to identify significant differences between species.

A repeated-measures design ANOVA and post hoc comparisons were employed to test for positional effects (proximal, middle and distal regions of the small intestine) on nutrient uptake rates and aminopeptidase-N activities. We used ANOVA to determine the postfeeding effects on nutrient uptake rates and aminopeptidase-N activity, and ANCOVA (body mass as the covariate) to test for postfeeding changes in total small intestinal capacity for nutrient uptake and aminopeptidase-N activity. Likewise, we used ANCOVA(body mass as the covariate) to test for postfeeding effects on intestinal mass, length and morphology, and the wet and dry masses of other organs. Species differences in intestinal morphology were also explored by ANCOVA and post hoc comparisons. We designate the level of significance as P<0.05 and report mean values as means ± 1 s.e.m.


Nerve Supply

As soon as food enters the mouth, it is detected by receptors that send impulses along the sensory neurons of cranial nerves. Without these nerves, not only would your food be without taste, but you would also be unable to feel either the food or the structures of your mouth, and you would be unable to avoid biting yourself as you chew, an action enabled by the motor branches of cranial nerves.

Intrinsic innervation of much of the alimentary canal is provided by the enteric nervous system, which runs from the esophagus to the anus, and contains approximately 100 million motor, sensory, and interneurons (unique to this system compared to all other parts of the peripheral nervous system). These enteric neurons are grouped into two plexuses. The myenteric plexus (plexus of Auerbach) lies in the muscularis layer of the alimentary canal and is responsible for motility, especially the rhythm and force of the contractions of the muscularis. The submucosal plexus (plexus of Meissner) lies in the submucosal layer and is responsible for regulating digestive secretions and reacting to the presence of food.

Extrinsic innervations of the alimentary canal are provided by the autonomic nervous system, which includes both sympathetic and parasympathetic nerves. In general, sympathetic activation (the fight-or-flight response) restricts the activity of enteric neurons, thereby decreasing GI secretion and motility. In contrast, parasympathetic activation (the rest-and-digest response) increases GI secretion and motility by stimulating neurons of the enteric nervous system.


Gastric Secretion: Mechanism and Hormones | Digestive System | Biology

In this article we will discuss about:- 1. Mechanism of Gastric Secretion 2. Hormones of Gastric Secretion 3. Effects of Various Chemicals and Drugs 4. Investigation.

Mechanism of Gastric Secretion:

The mechanism of gastric secretion has been chiefly studied on animals. Some direct evidence has been obtained in man, from cases of accidental gastric fistula through which gastric juice could be collected. In man another method is often applied known as fractional test meal. This method is commonly adopted for investigating gastric functions in man at bedside.

In animals two very important experiments have been done for investigating the mechanism of gastric secretion:

(1) The experiment of sham feeding, and

(2) The preparation of Pavlov’s pouch.

(Fig. 9.31). The oesophagus of a dog is exposed and divided in the middle of the neck and the two cut ends are brought to the surface. When the dog swallows food, the latter comes out through the upper cut end and does not enter the stomach. This experiment is very important to prove whether the food can stimulate gastric secretion even before entering stomach.

2. Pavlov’s Pouch (Fig. 9.32):

It is a small diverticulum prepared from the body of the stomach and representing about one-eighth of the whole stomach. The pouch is prepared in such a way that its inner end is shut off from the main cavity of the stomach by two layers of mucous membrane while the outer end opens outside through an wound in the abdominal wall. During the surgical procedure least injury is done to the vessels and nerves, so that the pouch secretes a juice identical with that secreted by the body of the stomach.

This preparation has got the following advantages:

i. Pure gastric juice can be collected from this pouch unmixed with food. This is a great help in studying the variations of gastric secretion—both in quality and quantity—as may be produced by different stimuli.

ii. It is found in dogs, that the juice secreted by the pouch is always a constant fraction of the total amount of juice secreted by the main stomach. From this the total secretion can be found out.

Hormones on Gastric Secretion:

Hormones secreted by different endocrine glands influence gastric secretion.

i. Glucocorticoids secreted by adrenal cortex stimulated by ACTH increases acid and pepsin secretion by the stomach but decrease the mucous secretion, and thus make it more susceptable to ulceration.

ii. Epinephrine and norepinephrine, on the other hand, decrease gastric secretion.

iii. Hypophysectomy causes characteristic changes in the chief cells of the gastric glands, consisting of a decrease in the size of nucleus and loss of most of the pepsinogen granules. Secretion of hydrochloric acid is also reduced.

iv. Serotonin, possibly a hormone secreted by certain enterochromaffin cells in the intestinal mucosa, inhibits gastric secretion particularly that activated reflexly or by cholinergic drugs.

v. Reserpine, which is used as a tranquiliser and in the treatment of high blood pressure, produces increased acid production in the stomach when given in a high dose for a long time. The mode of action is not clear.

vi. Insulin acts through its effect on glucose metabolism and has an effect on the gastric glands similar to that of stimulation of the vagi. Release of gastrin is reduced by insulin.

Effects of Various Chemicals and Drugs on Gastric Secretion:

Numerous chemical agents and various drugs affect gastric secretion.

i. Histamine is a powerful stimulant of gastric secretion. It is thought that it acts directly on the parietal cells. Histalog, an anlog of histamine, is also a powerful gastric stimulant.

ii. Caffeine and alcohol are strong secretory stimulants, producing a juice of high acidity and rich in mucin.

iii. Parasympathetic agents, such as acetylcholine, mecholyl, etc., are secretory stimulants.

iv. Secretory depressants are also known. Alkali and acids depress gastric secretion. Belladona, atropine, hyoscine, etc., are secretory depressants.

Investigation of Gastric Secretion in Man:

The method which is commonly adopted for investigating gastric secretion in man is called fractional test meal or gastric analysis.

The procedure is as follows:

The subject is given diet on the previous evening. In the next morning the patient is made to swallow a thin flexible rubber tube known as the stomach tube (Ryle’s tube, Lyon’s tube or some other modification, (Fig. 9.34). The tube has got three markings on it. When swallowed up to the first mark coinciding with incisor teeth (about 30 cm or 12 inches from the end) the end is near the cardiac end of the oesophagus if up to the second mark the end is within the stomach when up to the third mark the end has entered the duodenum.

During gastric analysis, the subject swallows the tube up to the second mark. The resting content of the stomach are aspirated out and is preserved. Then the patient takes about a pint of oat meal gruel, the stomach tube remaining swallowed as it was. Every fifteen minutes a sample of about 20 ml is drawn out and the procedure is continued for three hours. Altogether thirteen samples are obtained, the resting contents being the first sample.

Each sample is then tested for the following:

Normally the free HCI of the rest­ing contents lies between 1.5 and 2.0 mEq or 54 – 60 mgm (34.46 mgm = lmEq) of HCI. Af­ter the gruel is taken the acidity is reduced by dilution. The free HCI then steadily rises and becomes maximum 40 – 50 mEq of HCI in the second hour. Then it gradually declines. When bile enters due to regurgitation, gastric acidity is reduced (Fig. 9.35). In gastric ulcer the value increases up to 3 times.

This includes HCI com­bined with protein, mucus, etc., as well as or­ganic acids such as lactic acid, produced by fermentation. Normally it varies from 10-55 mEq of HCI. In hypochlorhydria or achlorhydria the rate of fermentation is more, so that, this Figure becomes high.

This is the sum total of free HCI organic acids, combined acid and acid salts.

This includes free HCI, com­bined HCI and inorganic chlorides. Its impor­tance lies in the fact that the free acid level is always disturbed by the entry of bile, but the total chlorides remain unaffected. Hence, esti­mation of total chlorides, along with estimation of free acidity, will give more correct information about the secreting capacity of stomach.

Sugar is produced by salivary digestion of starch. Presence of sugar and starch indicates that stomach has not yet completely emptied. Their absence, therefore, indicates the emptying time.

Normally, they are not found from the tenth or eleventh sample.

Presence of bile as indicated by yellow or green colour of the stomach contents shows duodenal regurgitation. It also indicates that pyloric sphincter has opened and gastric emptying has begun. Generally bile first appears in the second hour.

It is not a normal constituent. Its presence shows ulcer, cancer or other haemorrhagic conditions of stomach. In case of ulcer the blood might be bright red or brown in colour and in case of cancer it is brownish-black.

Derived mainly from fermentation of carbohydrate when there is a fall in the gastric hydrochloric acid. Hence, if free HCI is low, lactic acid will be high.

Excess of mucus indicates an irritated condition of the stomach. [Gastritis, etc.]

xi. Presence of Pepsin:

It indicates the functional condition of the peptic cells.

In addition to this, microscopic examination of each sample is carried out for blood cells, epithelial cells, tumour cells, bacteria, etc. Taking these facts into account a normal gastric analysis curve will be as shown in Fig. 9.36.

It will be seen from there that, this test not only gives an idea of the secreting capacity of stomach but the degree of motility (to be obtained from the emptying time), opening time of pylorus, duodenal regurgitation, etc., can be also known from it. In certain pathological condi­tions, characteristic variation of the curve is seen, viz., in gastric cancer and pernicious anaemia there will be achlorhydria, in duodenal ulcer the curve will be high ‘climbing’ type and so on.

To make a complete inves­tigation of gastric functions only fractional test meal is not enough radiological exam­ination after barium meal has also to be performed. This will show the size, shape, motility, emptying time, presence of ul­cer, etc., in the stomach.

Other Functional Tests:

Other functional tests of stom­ach are as follows:

i. Histamine Test of Gastric Secretion:

Histamine is a strong stimulant for the oxyntic cells. Only 0.5 mgm histamine chloride, injected subcutaneously, will stim­ulate gastric secretion at the rate of 200 ml per hour. In those patients who show achlorhydria with ordinary gastric analysis, this histamine test is performed in order to see the condition of the oxyntic cells. If per­formed in a normal subject, it shows the maximum secretory capacity of the oxyntic cells. Negative response indicates atrophy of oxyntic cells.

ii. Insulin Test of Gastric Secretion:

Insulin reduces blood sugar which in its turn, stimulates vagus and thereby excites gastric secretion. A positive insulin test is proof of the presence of intact vagal fibres but a negative result is less conclusive since some subjects with intact vagi fail to secrete in response to insulin.

However, the test is effective in most cases. Seven units of insulin given subcutaneously produce marked secretion of gastric juice (which is rich in HCI and pepsin content) although reduction of blood glucose by insulin to moderate degree causes inhibition of secretion. The secretion takes place after a latent period of 40 minutes.

This test also shows the secretory capacity of stomach. Since the response does not occur in absence of vagus so the absense of gastric secretion following insulin induced hypoglycaemia is a test for the vagal denervation. A combined insulin-histamine test (7 units of insulin, followed 20 minutes later by 0.5 mgm of histamine) is also advocated by some, to test the maximum secretory power of the gastric mucosa.

In about 2 – 5% of normal healthy people neither any HCI nor any pepsin is found in the gastric juice. This condition is called achylia gastrica. This is a congenital error due to non-development of oxyntic and peptic cells. This condition does not affect health. Because pancreatic enzymes can digest all the ingested foodstuffs. In certain pathological conditions (pernicious anaemia, cancer of the stomach, etc.), the acidity is very low (hypochlorhydria) or it may be altogether absent (achlorhydria).

On the other hand, some people may have higher acidity in the gastric juice (hyperchlorhydria). In females the acidity is proportionally lower than in males. In the infants and children it is much lower than in adults. In men after thirty and women after fifty both free and total acidity gradually decline. A high gastric acidity is generally associated with hypermotile stomach. In people with poor muscular built and sedentary habits the acidity is low.


Clinical Significance

Evaluatingਊ patient with LPR should always begin with a thorough history to determine the presence of suggesting symptoms such as chronic cough, hoarseness, dysphagia, or throat clearing. Since gastroesophageal reflux disease shares many similarities with LPR, the next step is to rule out GERD. symptoms that worsen while upright and during periods of physical exertion are more suggestive of LPR. On the other hand, symptoms that get worse while lying down are more indicative of GERD. An example would be nocturnal asthma-like symptoms in GERD. Another symptom that suggests GERD rather than LPR is retrosternal burning chest pain (heartburn). A laryngoscope aids in the diagnosis of LPR by showing posterior laryngeal edema or vocal cord edema.[7][9]

Treatment of LPR relies on a combination of dietary modification and pharmacological interventions. Dietary modifications include avoidance of acidic food such as citrus fruits, tomatoes, and salad dressings. Other dietary changes involve avoiding foods that can weaken the esophageal sphincters, including caffeine, peppermint, alcohol, chocolate, and fatty foods. When these interventions prove ineffective, adding a pharmacological treatment might help. The goal of treatment is to inhibit acid release from parietal cells. Recall that histamine is the primary stimulant of proton pumps in parietal cells. Therefore, histamine-blockers such as ranitidine and cimetidine can successfully suppress acid release, thereby decreasing pepsin activity.[11] Proton pump inhibitors are another class of acid-suppressing agents that work by directly inhibiting acid release. Examples of PPIs are omeprazole and esomeprazole.


24.1: Introduction to Digestive System Processes and Regulation - Biology

If you are like most people, you eat several meals and occasional snacks each day, but rarely think about the immense number of tasks that must be performed by your digestive system to break down, absorb and assimilate those nutrients. Robust control systems are required to coordinate digestive processes in man and animals, and are provided by both the nervous and endocrine systems. Endocrine control over digestive functions is provided by the so-called enteric endocrine system, which is summarized elsewhere.

The classical GI hormones are secreted by epithelial cells lining the lumen of the stomach and small intestine. These hormone-secreting cells - endocrinocytes - are interspersed among a much larger number of epithelial cells that secrete their products (acid, mucus, etc.) into the lumen or take up nutrients from the lumen. GI hormones are secreted into blood, and hence circulate systemically, where they affect function of other parts of the digestive tube, liver, pancreas, brain and a variety of other targets.

There are a large number of hormones, neuropeptides and neurotransmitters that affect gastrointestinal function. Interestingly, a number of the classical GI hormones are also synthesized in the brain, and sometimes referred to as "brain-gut peptides". The significance of this pattern of expression is not clear.

The following table summarizes the effects and stimuli for release of some major gastrointestinal hormones, each of which is discussed in more detail on subsequent pages:


Bile: Functions of Bile | Digestive Juice | Human Body | Biology

Bile is essential for life. Although it does not contain any enzyme, yet, it acts as a very important digestive juice. Its importance is so much that, life cannot be maintained without it. If a cannula is inserted in the common bile duct and all bile is collected outside, it is seen that the dog develops various abnormalities of bone, anaemia, lack of nutrition and eventually dies (Whipple).

Bile serves the following functions:

Bile is essential for the complete digestion of fats and to some extent of proteins and carbohy­drates.

This action is due to the presence of bile salts, which act in the following ways:

a. By reducing surface tension, so that fats are converted into an emulsion. The fine globules of fat, due to their innumerable number, render a larger surface area for the enzyme (lipase) to act. Due to this the process of digestion is quickened.

The bile salts, by virtue of the cholic acid radicle, act as a specific activator for different lipases. [That this action is not due to emulsification is proved by the fact that, although emulsification is unnecessary for the digestion of water-soluble triacetin by pancreatic lipase, yet the action of the enzyme is accelerated by bile salts.]

Bile acts as a good solvent. Due to this property, it serves as a good medium for the interacting fats and fat-splitting enzymes.

Bile helps in the absorption of various substances. This is also due to presence of bile salts.

The following things are absorbed with the help of bile:

Bile is essential for fat absorption.

This is carried out in two ways:

By this property the insoluble fatty acids, cholesterol, calcium, soaps, etc., – are made readily soluble in the watery contents of intestinal canal. In this way they are made easily diffusible and thus suitable for absorption. [This action is brought about by the combination of these substances with bile acids. Fatty acids, cholesterol and many such insoluble substances make loose compounds with desoxycholic acid. Such compounds are soluble in water and are called cholic acids.].

Bile salts reduce the surface tension of the absorbing epithelium, increase their permeability and thus facilitate absorption.

Iron, calcium and probably other mineral constituents of diet.

Bile salts help in the absorption of lipid-soluble vitamins A, D, E and K and pro-vitamin carotene.

Certain substances are excreted through bile, for instance:

i. Some metals like copper, zinc, mercury, etc.

iii. Bile pigments. [A portion of these pigments is then excreted in the faeces and in urine in various forms.]

iv. Cholesterol and lecithin are probably chiefly excretory products.

Bile salts stimulate peristalsis. When introduced directly into the colon it stimulates peristalsis of these parts.

Bile acts as its own stimulant. Bile salts are the strongest cholagogues. They are absorbed from intestine, carried to liver and stimulate further bile secretion. The taurocholate is stronger in this respect than the glycocholate.

6. Bile Helps to Maintain a Suitable pH:

Bile helps to maintain a suitable pH of the duodenal contents and thus helps the action of all the enzymes. Bile is an important source of alkali for neutralising the hydrochloric acid entering the intestine from stomach.

7. Lecithin and Cholesterol:

Lecithin and cholesterol, present in bile, also help in some ways:

First, they are treated as food and are reabsorbed.

Secondly, they act as adjuvants to bile salts in the process of emulsification of fats (but on the whole they are regarded as excreted products).

Mucin of bile acts as a buffer and a lubricant.

9. Regurgitation of Bile:

Regurgitation of bile in the stomach helps to neutralise gastric acidity and thus prevents the injurious effect of acids on gastric mucosa.

From the above it will be evident that bile is important not only as a digestive juice but for also various other purposes.


Discussion

Critique of methods

Although IR thermography has not seen widespread use in physiology, its non-invasive nature makes it an ideal method for rapidly assessing multiple surface temperatures in a large number of animals. The technology has reached the stage where resolution and the accuracy rival that of other temperature recording devices. The largest error in using this technique occurs in knowing the emissivity of the target. Most biological tissues exhibit an emissivity of 0.95, which implies that they emit 95% of the radiation emitted by an ideal blackbody radiator at the same temperature(Speakman and Ward, 1998). The emissivity of snake skin is unknown however, when IR image comparisons were made between the snakes' surface temperatures and the surface temperature of a substance of known emissivity, there were no discernable temperature differences, inferring that we have used a valid emissivity correction factor in the determination of surface temperatures.

Specific dynamic action and meal size effects on thermogenesis

By overlapping the thermal increment associated with feeding (present study) with the post-prandial metabolic response of rattlesnakes(Andrade et al., 1997), a clear correlation emerges between both variables (See Fig. 2). While digesting meal sizes 10–50% of their own body masses, this species experiences peaks in metabolism between 15 h and 33 h post-feeding, at values 3.7- to 7.3-fold higher than the values measured during fasting(Andrade et al., 1997). Similarly, we have found that thermogenesis attained greater magnitude in those snakes fed with larger meals and that the attainment of peak values in Tb occur in accordance with the peak in metabolism. It thus appears that the thermal effect of feeding that we recorded reflects a total body temperature increment arising from the SDA, as previously conjectured by Benedict(1932).

There are other possible explanations for the source of this heat production. Marcellini and Peters(1982) conjectured that undetectable muscular contractions and chemical decomposition of food may have contributed substantially to the post-prandial thermogenesis of snakes. Our data, however, suggest that the latter is unlikely. Indeed, we observed that a decaying, uneaten mouse produced no significant heat under the same experimental conditions (G. J. Tattersall, unpublished data). Further, the only increase in muscular activity that could be anticipated for digesting snakes is an increase in gut motility, since activity in general is decreased in fed snakes (Beck, 1996). This renders it improbable that an undetectable increase in muscular activity might have been involved in the increase in heat production after feeding. The maintenance of all snakes in a temperature-controlled room, with no possibility of changing heat exchange rates by behavioral means, excludes the possibility that the increment in body temperature exhibited by fed rattlesnakes is the result of an adjustment in thermoregulatory behavior, i.e. a post-prandial thermophilic response. Finally, the rattlesnakes' body temperatures returned to fasting levels with a time course that is in good agreement with the duration of the metabolic SDA response recorded for this species (Andrade et al.,1997).

Temperature effects on digestion and significance of thermogenesis

The benefits often associated with the post-prandial thermophilic response in reptiles include an increased rate of digestion and/or digestive efficiency(Stevenson et al., 1985 Lillywhite, 1987 Hailey and Davies, 1987 Reinert, 1993 Sievert and Andreadis, 1999)and an increase in gastrointestinal motility, secretion and absorption(Dandrifosse, 1974 Skoczylas, 1978 Mackay, 1968 Diefenbach, 1975a,bSkoczylas, 1970a,b). Moreover, temperature may affect chemical digestion more directly, since some digestive enzymes have maximal activity at higher temperatures(Licht, 1964). The general consequence of such temperature effects on digestion may be characterized by the shortening of the SDA duration at the expense of increased rates of metabolism (see Toledo et al.,2003 Wang et al.,2003). For snakes that ingest large meals and have their locomotor and defensive ability temporarily impaired, speeding up the digestive process through an increase in temperature may be especially relevant since it would reduce the risk of predation (Garland and Arnold, 1983 Ford and Shuttlesworth, 1986). Higher temperatures and faster digestion may also be accompanied by increased rates of food intake, as documented in skinks(Du et al., 2000), which will result in better body condition, growth and perhaps an increased fitness. Finally, the energetic cost of digestion itself seems to decrease at higher temperatures (Toledo et al.,2003).

For rattlesnakes, our results suggest that all beneficial consequences associated with the post-prandial thermophilic response listed above may be achieved not only by altering thermoregulatory behavior, but also through the thermogenic consequences of the elevated metabolism during digestion. In C. durissus, we have found that thermogenesis alone may account, on average, for a 0.9–1.2°C increase in body temperature during the first 2–3 days after feeding. The important question is whether such an increase would be of any physiological significance to the rattlesnake's digestion. We tried to address this issue by calculating the effect of a 1°C change in body temperature on the digestion of snakes, by regressing SDA duration and SDA cost (expressed as a percentage of the calorific content of the meal, i.e. SDA coefficient see Toledo et al., 2003) against body temperature, using a set of data obtained for C. durissus at 25° and 30°C (S. P. Brito, A. S. Abe and D. V. Andrade, unpublished data). This procedure revealed that a 1°C increase in body temperature,under the conditions in which we performed the experiments, may account for a 19 h decrease in SDA duration and a 0.3% decrease in the SDA coefficient. Thus, the thermogenic effect of feeding, per se, may, indeed, affect the digestive performance and the duration of digestion in rattlesnakes. Moreover, the ability to increase body temperature after feeding by thermoregulatory behaviors is reported to be constrained in rattlesnakes by the availability of adequate thermal microhabitats, reduced mobility and reclusive behaviors (Beck,1996). Thus, it seems possible that the beneficial effects of metabolic thermogenesis on digestion may assume a greater importance during the night, on cloudy days, or whenever behavioral thermoregulation and the achievement of the post-prandial thermophily are constrained. Finally, by using the infrared imaging technique, we assessed only body surface temperature and, therefore, differences in deep core body temperature due to digestion associated thermogenesis may be even larger. Indeed, in experiments performed with pythons fed with meals containing temperature data loggers,Marcellini and Peters (1982)were able to detect increases in body temperature up to 4°C (see also Benedict, 1932 Van Mierop and Barnard, 1976). Moreover, digesting pythons experience metabolic responses that are far larger than those observed in rattlesnakes(Andrade et al., 1997 Secor and Diamond, 2000),which could also contribute to the larger thermogenic effect of feeding exhibited by this species (Benedict,1932 Van Mierop and Barnard,1976 Marcellini and Peters,1982).

The thermogenic effect of feeding has been examined in one lizard species by Bennett et al. (2000) who found that digesting Varanus at 32 and 35° C tripled and quadrupled metabolic rate, respectively, but the resulting heat generated by such increases accounted for increases in body temperature of less than 1°C. This was mainly caused by the fact that the increased heat production was accompanied by increases in thermal conductance attributed to the greater ventilatory rates needed to support the higher rates of metabolism(Bennett et al., 2000). Although the same phenomenon may have prevented further increases in body temperature in C. durissus, the magnitude of this process in rattlesnakes most likely was smaller than that recorded in Varanus. Reptiles are known to exhibit a relative hypoventilation during digestion(Wang et al., 2001), but while the air convection requirement for O2 in Python was reduced by 46% (Secor et al.,2000), in Varanus this reduction was only 21.4%(Hicks et al., 2000). Thus,the heat loss due to the changes in conductance associated with the increased total ventilatory rates during digestion should have been greater for Varanus compared to C. durrisus. Finally, the larger thermogenic effect of feeding in rattlesnakes compared to Varanus may also be related to the larger metabolic response to feeding in C. durissus metabolism increases from 4- to 7-fold(Andrade et al., 1997),compared to a 3- to 4-fold change seen in Varanus(Bennett et al., 2000).

In brooding pythons Python molurus body temperature can increase up to 7.3°C above ambient temperature by endogenous heat production, due to increased metabolic rates associated with the spasmodic contractions of the body musculature (Hutchison et al.,1966). This figure is far more impressive than the thermogenic effect of feeding found in rattlesnakes (present study) and in varanid lizards(Bennett et al., 2000). Interestingly, however, brooding pythons showing such a large increase in body temperature experience metabolic rates that are only 9.3 times higher than non-brooding females under the same environmental conditions(Hutchison et al., 1966). Thus, the discrepancy between the increase in metabolism and body temperature among brooding pythons and digesting rattlesnakes and lizards indicates that other factors may affect the thermoregulatory ability of brooding pythons. One likely factor is posture by remaining coiled around the eggs, brooding pythons decrease the surface area, which otherwise would serve as an avenue for heat loss (see Vinegar et al.,1970). Other possibilities are changes in conductance associated with circulatory adjustments, however, changes in heat transport viathe circulatory system remain to be investigated.

Concluding remarks

Endotherms may use SDA or exercise-generated heat for thermogenesis, saving a substantial amount of energy that would otherwise be used for this purpose(Costa and Kooyman, 1984). For an ectotherm, the general notion is that the heat generated during digestion is a wasteful byproduct generated from the metabolic increment(Hailey and Davies, 1987)since they naturally do not use metabolism to generate heat for thermoregulation. However, thermogenesis in snakes may act in concert with the behavioral post-prandial thermophilic response to achieve the suite of ecological and energetic benefits of increased body temperature during digestion. Particularly poignant in the case of snakes is the long, protracted digestion process. So, although the magnitude of the thermal increment following feeding may seem negligible, the duration of this sustained increase in body temperature is sufficient to suggest that digestion-derived heat in this ectotherm is a physiologically and ecologically important phenomenon.


Watch the video: An Introduction to the Digestive System (October 2022).