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)

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.

scholarly journals Enteral arginase II provides ornithine for citrulline synthesis

2011 ◽  
Vol 300 (1) ◽  
pp. E188-E194 ◽  
Author(s):  
Juan C. Marini ◽  
Bettina Keller ◽  
Inka Cajo Didelija ◽  
Leticia Castillo ◽  
Brendan Lee
Keyword(s):  
Small Intestine ◽  
Stable Isotope ◽  
Transgenic Mice ◽  
Small Intestinal Mucosa ◽  
Wild Type ◽  
Proline Utilization ◽  
Small Intestinal ◽  
Arginase Ii ◽  
Citrulline Synthesis

The synthesis of citrulline from arginine in the small intestine depends on the provision of ornithine. To test the hypothesis that arginase II plays a central role in the supply of ornithine for citrulline synthesis, the contribution of dietary arginine, glutamine, and proline was determined by utilizing multitracer stable isotope protocols in arginase II knockout (AII−/−) and wild-type (WT) mice. The lack of arginase II resulted in a lower citrulline rate of appearance (121 vs. 137 μmol·kg−1·h−1) due to a reduced availability of ornithine; ornithine supplementation was able to restore the rate of citrulline production in AII−/− to levels comparable with WT mice. There were significant differences in the utilization of dietary citrulline precursors. The contribution of dietary arginine to the synthesis of citrulline was reduced from 45 to 10 μmol·kg−1·h−1 due to the lack of arginase II. No enteral utilization of arginine was observed in AII−/− mice (WT = 25 μmol·kg−1·h−1), and the contribution of dietary arginine through plasma ornithine was reduced in the transgenic mice (20 vs. 13 μmol·kg−1·h−1). Dietary glutamine and proline utilization were greater in AII−/− than in WT mice (20 vs. 13 and 1.4 vs. 3.7 μmol·kg−1·h−1, respectively). Most of the contribution of glutamine and proline was enteral rather than through plasma ornithine. The arginase isoform present in the small intestinal mucosa has the role of providing ornithine for citrulline synthesis. The lack of arginase II results in a greater contribution of plasma ornithine and dietary glutamine and proline to the synthesis of citrulline.

Rapid synthesis and secretion of intestinal apolipoprotein A-IV after gastric fat loading in rats

1997 ◽  
Vol 272 (4) ◽  
pp. R1170-R1177 ◽  
Author(s):  
M. D. Rodriguez ◽  
T. J. Kalogeris ◽  
X. L. Wang ◽  
R. Wolf ◽  
P. Tso
Keyword(s):  
Small Intestine ◽  
Food Intake ◽  
Intragastric Administration ◽  
Short Term ◽  
Apolipoprotein A ◽  
Inhibit Food Intake ◽  
Rapid Stimulation ◽  
Kinetics Of ◽  
Distal Jejunum

To further investigate the possible role of apolipoprotein A-IV (apo A-IV) in the short-term control of food intake, we examined the kinetics of intestinal apo A-IV synthesis and release into lymph and plasma after intragastric delivery of physiological amounts of lipid. Within 30 min of intragastric administration of 0.1 g of triglyceride, plasma and lymph levels of apo A-IV were similar to those produced by exogenous apo A-IV that inhibit food intake. Within 15 min, 5% of gastrically delivered radioactive lipid reached the distal small bowel and cecum; by 30 min radioactivity was evenly distributed throughout the small intestine, with 10-15% of the load in the distal gut. By 30 min, synthesis of apo A-IV was significantly stimulated in proximal and distal jejunum and distal ileum and remained elevated up to 4 h after the delivery of lipid. Our results indicate that the delivery of physiological amounts of lipid into the stomach produces a significant and rapid stimulation of apo A-IV secretion into lymph and plasma, together with a rapid delivery of lipid and increases in mucosal synthesis of apo A-IV along the entire length of the small intestine. The results support a possible role for apo A-IV in the short-term control of food intake and suggest a role for the entire gut in the integrative response of apo A-IV to a fat meal.

scholarly journals Postgraduate Symposium The role of fat in gastric emptying and satiety: acute and chronic effects

2009 ◽  
Vol 68 (1) ◽  
pp. 89-97 ◽  
Author(s):  
Miriam Clegg ◽  
Amir Shafat
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Gastrointestinal Transit ◽  
Positive Energy ◽  
Low Fat ◽  
Low Fat Diet ◽  
The Metabolic Syndrome ◽  
Increase Food Intake ◽  
Positive Energy Balance

Dietary fat is an important factor in the aetiology of obesity and the metabolic syndrome. It has been widely debated whether gastric emptying (GE) is altered in obesity. GE times have been reported as both longer and shorter in obese individuals compared with matched lean individuals. However, the general consensus is that GE is accelerated and satiety is lower in obesity. Research has implicated a high-fat (HF) diet in these findings. A single HF meal has a longer GE time than a low-fat meal and can even delay GE of the subsequent meal. However, an HF diet has shown different effects. Feeding a HF diet adapts gastrointestinal function to reduce GE times in comparison with a low-fat diet. Increased GE may lead to decreased satiety and faster onset of subsequent eating episodes. Further results have suggested that consuming an HF diet for 14 d increases the GE rate of HF food but not low-fat food. Consuming HF diets for 2 weeks has also been shown to increase food intake. Decreased satiation following an HF diet may cause increased food intake and a positive energy balance, potentially resulting in a gradual increase in adiposity. Recent results have suggested that gastrointestinal transit is accelerated following only 3 d on a HF diet. The variable GE times reported in obesity may be associated with interactions between the HF diet and obesity and not simply the obese state.

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.

Role of Ca2+ in non-cholinergic, non-adrenergic responses to nerve stimulation of the guinea-pig small intestine

1982 ◽  
Vol 319 (2) ◽  
pp. 115-120 ◽  
Author(s):  
V. Bauer ◽  
O. Matušák ◽  
M. Bezeková ◽  
L. Beneš ◽  
H. Kuriyama
Keyword(s):  
Small Intestine ◽  
Guinea Pig ◽  
Nerve Stimulation ◽  
Stimulation Of

scholarly journals Gs-coupled GPCR signalling in AgRP neurons triggers sustained increase in food intake

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Ken-ichiro Nakajima ◽  
Zhenzhong Cui ◽  
Chia Li ◽  
Jaroslawna Meister ◽  
Yinghong Cui ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Potential Role ◽  
G Protein Coupled Receptors ◽  
Signalling Cascades ◽  
Treatment Of Obesity ◽  
G Protein Coupled ◽  
Stimulation Of ◽  
Sustained Increase

Abstract Agouti-related peptide (AgRP) neurons of the hypothalamus play a key role in regulating food intake and body weight, by releasing three different orexigenic molecules: AgRP; GABA; and neuropeptide Y. AgRP neurons express various G protein-coupled receptors (GPCRs) with different coupling properties, including Gs-linked GPCRs. At present, the potential role of Gs-coupled GPCRs in regulating the activity of AgRP neurons remains unknown. Here we show that the activation of Gs-coupled receptors expressed by AgRP neurons leads to a robust and sustained increase in food intake. We also provide detailed mechanistic data linking the stimulation of this class of receptors to the observed feeding phenotype. Moreover, we show that this pathway is clearly distinct from other GPCR signalling cascades that are operative in AgRP neurons. Our data suggest that drugs able to inhibit this signalling pathway may become useful for the treatment of obesity.

scholarly journals Expression of proposed methionine transporters along the gastrointestinal tract of pigs and their regulation by dietary methionine sources

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Stella Romanet ◽  
Jörg R. Aschenbach ◽  
Robert Pieper ◽  
Jürgen Zentek ◽  
John K. Htoo ◽  
...  
Keyword(s):  
Small Intestine ◽  
Gastrointestinal Tract ◽  
Protein Expression ◽  
Mrna Expression ◽  
Oral Mucosa ◽  
Protein Translation ◽  
Primary Role ◽  
Intestinal Segments ◽  
Small Intestinal

Abstract Background Given the key role of methionine (Met) in biological processes like protein translation, methylation, and antioxidant defense, inadequate Met supply can limit performance. This study investigated the effect of different dietary Met sources on the expression profile of various Met transporters along the gastrointestinal tract (GIT) of pigs. Methods A total of 27 pigs received a diet supplemented with 0.21% DL-Met, 0.21% L-Met, or 0.31% DL-2-hydroxy-4-(methylthio)butanoic acid (DL-HMTBA). Changes in mRNA expression of B0AT1, ATB0,+, rBAT, ASCT2, IMINO, LAT4, y+LAT1, LAT2, and SNAT2 were evaluated in the oral mucosa, cardia, fundus, pylorus, duodenum, proximal jejunum, middle jejunum, ileum, cecum, proximal colon, and distal colon, complemented by protein expression analysis of B0AT1, ASCT2, LAT2, and LAT4. Results Expression of all investigated transcripts differed significantly along the GIT. B0AT1, rBAT, y+LAT1, LAT2, and LAT4 showed strongest mRNA expression in small intestinal segments. ASCT2, IMINO, and SNAT2 were similarly expressed along the small and large intestines but expression differed in the oral mucosa and stomach. ATB0,+ showed highest mRNA expression in large intestinal tissues, cardia, and pylorus. In pigs fed DL-Met, mRNA expression of ASCT2 was higher than in pigs fed DL-HMTBA in small intestinal tissues and mRNA expression of IMINO was lower than in pigs fed L-Met in large intestinal tissues. Dietary DL-HMTBA induced a stronger mRNA expression of basolateral uptake systems either in the small (LAT2) or large (y+LAT1) intestine. Protein expression of B0AT1 was higher in the middle jejunum and ileum in pigs fed DL-Met when compared with the other Met supplements. LAT4 expression was higher in pigs fed DL-HMTBA when compared with DL-Met (small intestine) and L-Met (small intestine, oral mucosa, and stomach). Conclusion A high expression of several Met transporters in small intestinal segments underlines the primary role of these segments in amino acid absorption; however, some Met transporters show high transcript and protein levels also in large intestine, oral mucosa, and stomach. A diet containing DL-Met has potential to increase apical Met transport in the small intestine, whereas a diet containing DL-HMTBA has potential to increase basolateral Met transport in the small intestine and, partly, other gastrointestinal tissues.

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