Stimulation of Gastric Transit Function Driven by Hydrolyzed Casein Increases Small Intestinal Carbohydrate Availability and Its Microbial Metabolism

2020 ◽  
Vol 64 (21) ◽  
pp. 2000250
Author(s):  
Junhua Shen ◽  
Chunlong Mu ◽  
Huisong Wang ◽  
Zan Huang ◽  
Kaifan Yu ◽  
...  
Keyword(s):  
Microbial Metabolism ◽  
Carbohydrate Availability ◽  
Small Intestinal ◽  
Stimulation Of

Effect of food intake on intestinal cholesterol synthesis in rats

1986 ◽  
Vol 251 (3) ◽  
pp. G362-G369
Author(s):  
K. R. Feingold ◽  
G. Zsigmond ◽  
S. R. Lear ◽  
A. H. Moser
Keyword(s):  
Small Intestine ◽  
Food Intake ◽  
Direct Contact ◽  
Cholesterol Synthesis ◽  
Third Trimester ◽  
Increase Food Intake ◽  
Effect Of Food ◽  
Small Intestinal ◽  
Stimulation Of

The mechanism by which diabetes results in an increase in small intestinal cholesterol synthesis is unknown. Previous studies have demonstrated that limiting food intake prevents the increase in intestinal cholesterol synthesis, and it has therefore been proposed that the stimulation of cholesterol synthesis in the small intestine is secondary to the hyperphagia that is associated with poorly controlled diabetes. To shed further light on the role of hyperphagia we have studied the effect on cholesterol synthesis of a variety of conditions that increase food intake. In third-trimester pregnant animals, lactating animals, obese animals, and in animals infused intragastrically with 16 g glucose/day vs. 8 g glucose/day, we have observed that an increase in food intake is associated with an increase in small intestinal cholesterol synthesis. Furthermore, these findings support the hypothesis that hyperphagia is the chief stimulus for the increase in cholesterol synthesis in the small intestine of diabetic animals. Additional studies have demonstrated that simply increasing the bulk of food ingested by adding Alphacel to the diet does not alter cholesterol synthesis in the small intestine. Lastly, in animals in whom Thiry fistulas were surgically constructed we observed that cholesterol synthesis is increased in the diabetic animals in both the segment of the small intestine in contact with the food stream and the segment of the small intestine that is excluded from contact. This observation suggests that the direct contact of the intestinal mucosa with caloric sources is not the sole trigger for increasing small intestinal cholesterol synthesis in hyperphagic diabetic animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Roles of Cyclooxygenase, Prostaglandin E2 and EP Receptors in Mucosal Protection and Ulcer Healing in the Gastrointestinal Tract

2018 ◽  
Vol 24 (18) ◽  
pp. 2002-2011 ◽  
Author(s):  
Koji Takeuchi ◽  
Kikuko Amagase
Keyword(s):  
Acid Reflux ◽  
Mucus Secretion ◽  
Gastric Ulcers ◽  
Bacterial Invasion ◽  
Mucosal Protection ◽  
Promoting Effect ◽  
Protective Mechanisms ◽  
Intestinal Lesions ◽  
Small Intestinal ◽  
Stimulation Of

Endogenous prostaglandins (PGs), produced from arachidonic acid by the two isoforms of cyclooxygenase (COX), play a pivotal role in maintaining mucosal integrity by modulating various functions of the gastrointestinal (GI) tract, and PGE2 is most effective in these actions. The PGE2 receptor is classified into 4 specific G-protein coupled subtypes, EP1-EP4, and their distribution accounts for the multiple effects of this prostanoid. PGE2 prevents acid-reflux esophagitis and indomethacin-induced gastric lesions through EP1 receptors, while endogenous PGs protect the stomach against cold restraint stress mediated by mainly PGI2/IP receptors and partly EP4 receptors. PGE2 also exhibits a protective effect against acid-induced duodenal damage and indomethacin-induced small intestinal lesions mediated by EP3/EP4 receptors; these effects in the stomach, duodenum, or small intestine are associated functionally with inhibition of gastric contraction (EP1), stimulation of duodenal HCO3 - secretion (EP3/EP4), or suppression of bacterial invasion due to the inhibition of intestinal motility (EP4) as well as stimulation of mucus secretion (EP3/EP4), respectively. PGE2 also prevents ischemiainduced enteritis and dextran sulfate sodium-induced colitis mediated by EP4 receptors, and the protective mechanisms may be related to the stimulation of mucus secretion and the down-regulation of immune response, respectively. Furthermore, PGE2 shows a healing-promoting effect on gastric ulcers and small intestinal lesions through the up-regulated expression of vascular endothelial growth factor (VEGF) and stimulation of angiogenesis via the activation of EP4 receptors. Finally, COX-1 is mainly responsible for the production of endogenous PGs involved in mucosal protection, while COX-2 is mainly responsible for those involved in the healing of gastric ulcers or small intestinal lesions. These findings contribute to future development of new strategies for the treatment of GI diseases.

Localization of cholesterol synthesis in the small intestine of diabetic rats

1984 ◽  
Vol 247 (5) ◽  
pp. G494-G501
Author(s):  
K. R. Feingold ◽  
A. H. Moser
Keyword(s):  
Diabetes Mellitus ◽  
Small Intestine ◽  
Food Intake ◽  
Cholesterol Synthesis ◽  
Diabetic Rats ◽  
Cholesterol Feeding ◽  
Small Intestinal ◽  
Stimulation Of ◽  
Do So

Previous studies have demonstrated that cholesterol synthesis is increased twofold in the small intestine of diabetic animals. The present study demonstrates that the stimulation of small intestinal cholesterol synthesis by diabetes is a generalized phenomenon occurring in all segments of the small intestine. Quantitatively, in control animals the proximal two segments of the small intestine account for the majority of the total small intestinal cholesterol synthesis, whereas in the diabetic animals, because of the generalized stimulation in cholesterogenesis, the contribution of the terminal segments to total small intestinal cholesterol synthesis is of increased importance. The various manipulations that regulate cholesterol synthesis in the small intestine of diabetic animals also affect cholesterol synthesis in all portions of the small intestine. In diabetic animals cholesterol feeding and the limitation of food intake decrease cholesterol synthesis in the total small intestine and in all segments of the small intestine. Conversely, colestipol feeding increases cholesterol synthesis in all segments of the small intestine. These results demonstrate that, despite the obvious structural, functional, and environmental differences among the various segments of the small intestine, the stimulation of cholesterol synthesis that occurs secondary to diabetes mellitus is a generalized phenomenon. Similarly, the factors that regulate small intestinal cholesterol synthesis do so in a generalized manner.

In birds, NHE2 is major brush-border Na+/H+exchanger in colon and is increased by a low-NaCl diet

1998 ◽  
Vol 274 (6) ◽  
pp. R1659-R1669 ◽  
Author(s):  
M. Donowitz ◽  
C. De La Horra ◽  
M. L. Calonge ◽  
I. S. Wood ◽  
J. Dyer ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Brush Border ◽  
Glucose Transporter ◽  
Plasma Aldosterone ◽  
Differential Sensitivity ◽  
Colonic Epithelial Cells ◽  
Brush Borders ◽  
Small Intestinal ◽  
Increased Activity ◽  
Stimulation Of

We previously reported that mammalian small intestinal and colonic brush borders (BBs) contained both epithelial Na+/H+exchangers NHE2 and NHE3. We now show that, in the avian (chicken) colon, NHE2 is the major functional isoform under basal conditions and when stimulated by a low-NaCl diet. Hubbard chickens were maintained for 2 wk on a high- or low-NaCl diet. After the chickens were killed, the ileum and colon were removed, and BBs were prepared by Mg2+ precipitation and22Na andd-[14C]glucose uptake determined in the BB vesicles. NHE2 and NHE3 were separated by differential sensitivity to HOE-694 (NHE2 defined as Na+/H+exchange inhibited by 50 μM HOE-694). Chickens on a low-Na+ diet have increased plasma aldosterone (10 vs. 207 pg/ml). On the high-NaCl diet, both NHE2 and NHE3 contributed to ileal and colonic apical Na+/H+exchange, contributing equally in ileum, but NHE2 being the major component in colon (86%). Low-NaCl diet significantly increased ileal and colonic BB Na+/H+exchange; the increase in BB Na+/H+exchange in both ileum and colon was entirely due to an increase in NHE2 with no change in NHE3 activity. In contrast, low-NaCl diet decreased ileal and colonic Na+-dependentd-glucose uptake. Western analysis showed that low-Na+ diet increased the amount of NHE2 in the ileal and colonic BB and decreased the amount of ileal Na+-dependent glucose transporter SGLT1. Both NHE2 and NHE3 were present in the apical but not basolateral membranes (BLM) of ileal and colonic epithelial cells. In summary, 1) NHE2 and NHE3 are both present in the BB and not BLM of chicken ileum and colon; 2) NHE2 is the major physiological colonic BB Na+/H+exchanger under basal conditions; 3) low-NaCl diet, which increases plasma aldosterone, increases ileal and colonic BB Na+/H+exchange and decreases Na+-dependentd-glucose uptake; 4) the stimulation of colonic BB Na+/H+exchange is due to increased activity and amount of NHE2; and 5) the inhibition of ileald-glucose uptake is associated with a decrease in SGLT1 amount. NHE2 is the major chicken colonic BB Na+/H+exchanger.

scholarly journals Differential stimulation of S-adenosylmethionine decarboxylase by difluoromethylornithine in the rat colon and small intestine

1989 ◽  
Vol 259 (2) ◽  
pp. 513-518 ◽  
Author(s):  
A G Halline ◽  
P K Dudeja ◽  
T A Brasitus
Keyword(s):  
Small Intestine ◽  
Specific Inhibitor ◽  
Product Inhibition ◽  
Rat Colon ◽  
Decarboxylase Activity ◽  
Adenosylmethionine Decarboxylase ◽  
Small Intestinal ◽  
Inhibition Studies ◽  
Small And Large Intestine ◽  
Stimulation Of

The effects of chronic inhibition of ornithine decarboxylase (ODC) by the specific inhibitor difluoromethylornithine (DFMO) in the rat colon and small intestine on mucosal contents of polyamines, decarboxylated S-adenosylmethionine (decarboxylated AdoMet) and S-adenosylmethionine decarboxylase (AdoMet decarboxylase) activity were studied. Administration of 1% DFMO in the drinking water for 10 or 15 weeks resulted in inhibition of ODC and decreases in intracellular putrescine and spermidine contents in both proximal and distal segments of small intestine and colon. At both time points DFMO administration resulted in a dramatic stimulation of AdoMet decarboxylase activity and a rise in decarboxylated AdoMet content in the proximal and distal small-intestinal segments compared with controls, which was not seen in either colonic segment of DFMO-treated animals. This differential stimulation of AdoMet decarboxylase by DFMO in the small intestine and colon could not be entirely explained on the basis of differences in polyamine contents, which are known to regulate this enzyme activity. Kinetic and inhibition studies of AdoMet decarboxylase in control small and large intestine revealed that: (1) there was no difference in Vmax. values between the tissues; (2) the Km for AdoMet was higher in the small intestine than in the colon; and (3) the Ki for product inhibition by decarboxylated AdoMet was higher in the small intestine than in the colon. These results suggest that the differential stimulation of AdoMet decarboxylase by DFMO in the small intestine and colon may be due to different isoenzymes and could play a significant role in the regulation of polyamine contents throughout the gut.

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