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.

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)

Total gastrectomy and small intestinal cholesterol synthesis in diabetic rats

Diabetes ◽  
1989 ◽  
Vol 38 (2) ◽  
pp. 219-224
Author(s):  
K. R. Feingold ◽  
Q. H. Zeng ◽  
M. Soued ◽  
A. Siperstein ◽  
M. K. Serio ◽  
...  
Keyword(s):  
Total Gastrectomy ◽  
Cholesterol Synthesis ◽  
Diabetic Rats ◽  
Small Intestinal

scholarly journals Chlamydia Deficient in Plasmid-Encoded pGP3 Is Prevented from Spreading to Large Intestine

2020 ◽  
Vol 88 (6) ◽  
Author(s):  
Zhi Huo ◽  
Conghui He ◽  
Ying Xu ◽  
Tianjun Jia ◽  
Jie Wang ◽  
...  
Keyword(s):  
Small Intestine ◽  
Gastrointestinal Tract ◽  
Large Intestine ◽  
Oral Inoculation ◽  
Mouse Small Intestine ◽  
Small Intestinal ◽  
Gastric Barrier ◽  
Better Than ◽  
Do So ◽  
Live Organism

ABSTRACT The cryptic plasmid pCM is critical for chlamydial colonization in the gastrointestinal tract. Nevertheless, orally inoculated plasmid-free Chlamydia sp. was still able to colonize the gut. Surprisingly, orally inoculated Chlamydia sp. deficient in only plasmid-encoded pGP3 was no longer able to colonize the gut. A comparison of live organism recoveries from individual gastrointestinal tissues revealed that pGP3-deficient Chlamydia sp. survived significantly better than plasmid-free Chlamydia sp. in small intestinal tissues. However, the small intestinal pGP3-deficient Chlamydia sp. failed to reach the large intestine, explaining the lack of live pGP3-deficient Chlamydia sp. in rectal swabs following an oral inoculation. Interestingly, pGP3-deficient Chlamydia sp. was able to colonize the colon following an intracolon inoculation, suggesting that pGP3-deficient Chlamydia sp. might be prevented from spreading from the small intestine to the large intestine. This hypothesis is supported by the finding that following an intrajejunal inoculation that bypasses the gastric barrier, pGP3-deficient Chlamydia sp. still failed to reach the large intestine, although similarly inoculated plasmid-free Chlamydia sp. was able to do so. Interestingly, when both types of organisms were intrajejunally coinoculated into the same mouse small intestine, plasmid-free Chlamydia sp. was no longer able to spread to the large intestine, suggesting that pGP3-deficient Chlamydia sp. might be able to activate an intestinal resistance for regulating Chlamydia sp. spreading. Thus, the current study has not only provided evidence for reconciling a previously identified conflicting phenotype but also revealed a potential intestinal resistance to chlamydial spreading. Efforts are under way to further define the mechanism of the putative intestinal resistance.

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.

Total Gastrectomy and Small Intestinal Cholesterol Synthesis in Diabetic Rats

Diabetes ◽  
1989 ◽  
Vol 38 (2) ◽  
pp. 219-224 ◽  
Author(s):  
K. R. Feingold ◽  
Q.-H. Zeng ◽  
M. Soued ◽  
A. Siperstein ◽  
M. K. Serio ◽  
...  
Keyword(s):  
Total Gastrectomy ◽  
Cholesterol Synthesis ◽  
Diabetic Rats ◽  
Small Intestinal

Localization of cholesterol synthesis along villus-crypt axis in diabetic rats

1987 ◽  
Vol 253 (3) ◽  
pp. G336-G344
Author(s):  
K. R. Feingold ◽  
A. H. Moser
Keyword(s):  
Small Intestine ◽  
Cholesterol Synthesis ◽  
Cell Mass ◽  
Diabetic Rats ◽  
Major Site ◽  
Distal Small Intestine ◽  
Proximal Small Intestine ◽  
Cell Layers ◽  
Cell Fractions ◽  
Crypt Cells

In diabetic animals cholesterol synthesis is increased in the small intestine, and this increase occurs in all segments along the duodenal-ileal axis. In the present study we have determined the sites along the villus-crypt axis in which cholesterol synthesis is increased. In diabetic animals cholesterol synthesis is increased in the proximal small intestine, and this is chiefly due to an increased synthesis in the crypt cells. In the midintestine cholesterol synthesis is increased in all cell fractions, but again the crypt cells are the major site accounting for the increase. In the distal small intestine synthesis is increased in all cell fractions, but the increase is greatest in the upper villus cells. Thus the basis for the increase in intestinal cholesterol synthesis in diabetic animals is dependent on location. Additionally, in the proximal small intestine the increase in synthesis is due to an increased mass of cells, whereas in the distal small intestine the increase is due to an increased synthesis per unit of tissue. In cholesterol-fed diabetic animals we observed a decrease in cholesterol synthesis in the proximal and midintestine that was due to a decrease in synthesis in all cell fractions. This decrease in synthesis is accounted for by a decrease in synthesis per unit of tissue. Restricting food intake in the diabetic animals decreased cholesterol synthesis in all cell layers, and this decrease is due to a decrease in cell mass.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of a chronic subclinical infection ofTrichostrongylus colubriformison gastrointestinal motility and digesta flow in sheep

Parasitology ◽  
1985 ◽  
Vol 91 (2) ◽  
pp. 381-396 ◽  
Author(s):  
P. C. Gregory ◽  
G. Wenham ◽  
D. Poppi ◽  
R. L. Coop ◽  
J. C. MacRae ◽  
...  
Keyword(s):  
Small Intestine ◽  
Food Intake ◽  
Transit Time ◽  
Gastrointestinal Motility ◽  
Subclinical Infection ◽  
Intestinal Transit Time ◽  
Small Intestinal Transit ◽  
Proximal Small Intestine ◽  
Small Intestinal ◽  
Small Intestinal Transit Time

The influence of a chronic subclinicael infection ofTrichostrongylus colubriformis, 2500 larvae/day for 12 weeks, on gastrointestinal motility and digesta flow was studied in 12 sheep suppliedad libitumwith food and water. Motility was recorded by X-radiography and electromyography from chronically implanted electrodes;abomasal volume and outflow were estimated by dilution of CrEDTA; small intestinal transit time was estimated by passage of Phenol Red. The findings were compared with measurements made prior to infection at restricted food intake and reported separately. The first effects of infection were seen after 3–4 weeks. No animal developed diarrhoea, but food intake was progressively reduced. Small intestinal transit time, abomasal volume and half-time of marker dilution increased while abomasal outflow decreased during infection. These changes occurred both in absolute terms and when compared with values predicted from the observed level of food intake. As the animals became resistant to the parasites abomasal volume and digesta flow returned towards control values (weeks 10–12). The migrating myoelectric complex (MMC) was disrupted in only one sheep, and only transiently. In all sheep the frequency of the MMC was increased during infection and there was a progressive inhibition of abomasal, duodenal and jejunal motility. X-radiography showed there was prolonged pooling of digesta in the proximal small intestine which was cleared only at the phase of regular spiking activity. Two sheep given an anthelmintic drench recovered normal motility and clearance of digesta. It is concluded that subclinical infection of sheep with T.colubriformisalters the normal pattern of gastrointestinal motility in the absence of any diarrhoea, and causes inhibition of abomasal and proximal small intestinal motility and digesta flow. The increased frequency of MMCs helps to maintain digesta flow through the proximal small intestine.

Mechanism of impaired responses of cerebral arterioles during diabetes mellitus

1991 ◽  
Vol 260 (2) ◽  
pp. H319-H326 ◽  
Author(s):  
W. G. Mayhan ◽  
L. K. Simmons ◽  
G. M. Sharpe
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Receptor Antagonist ◽  
Intravital Microscopy ◽  
Diabetic Rats ◽  
H2 Receptor Antagonist ◽  
Pial Arterioles ◽  
Cerebral Arterioles ◽  
Arteriolar Diameter ◽  
Stimulation Of

The goal of this study was to determine the mechanism of impaired responses of cerebral arterioles during diabetes mellitus. To induce diabetes, rats were injected with streptozotocin. Rats were characterized as diabetic by a blood glucose of greater than 300 mg/dl. Diameter of pial arterioles was measured with intravital microscopy in nondiabetic and diabetic rats during superfusion with acetylcholine (ACh), ADP, the thromboxane (Tx) analogue U-46619, and nitroglycerin. ACh increased pial arteriolar diameter in nondiabetic rats and did not alter diameter in diameter in diabetic rats. ADP increased pial arteriolar diameter in nondiabetic rats and produced minimal changes in diameter of arterioles in diabetic rats. Tx analogue U-46619 produced similar constriction of cerebral arterioles in nondiabetic and diabetic rats. In addition, nitroglycerin produced similar dilatation of cerebral arterioles in nondiabetic and diabetic rats, suggesting that impaired dilatation of cerebral arterioles in diabetic rats was not related to nonspecific impairment of vasodilatation. Next, we examined the possibility that impaired responses of cerebral arterioles in diabetic rats in response to ACh and ADP may be related to production of a cyclooxygenase constrictor substance. Indomethacin and the TxA2-prostaglandin (PG) H2 receptor antagonist SQ 29548 restored dilator responses to ACh and ADP in diabetic rats toward that observed in nondiabetic rats. Indomethacin and SQ 29548 did not alter responses in nondiabetic rats. Thus diabetes mellitus impairs endothelium-dependent responses of cerebral arterioles. The mechanism of impaired responses of cerebral arterioles during diabetes mellitus appears to be related to the production of a cyclooxygenase constrictor substance and presumably related to stimulation of the TxA2-PGH2 receptor.

scholarly journals Effect of Macronutrient Type and Gastrointestinal Release Site on PYY Response in Normal Healthy Subjects

2019 ◽  
Vol 104 (9) ◽  
pp. 3661-3669 ◽  
Author(s):  
Aisling M Mangan ◽  
Werd Al Najim ◽  
Niamh McNamara ◽  
William P Martin ◽  
Andrius Antanaitis ◽  
...  
Keyword(s):  
Small Intestine ◽  
Food Intake ◽  
Healthy Subjects ◽  
Release Site ◽  
Distal Small Intestine ◽  
Intestinal Delivery ◽  
Ad Libitum ◽  
Small Intestinal ◽  
Double Blinded ◽  
Test Drink

Abstract Background and Aims Enteroendocrine L cells release satiety inducing hormones in response to stimulation by luminal macronutrients. We sought to profile the differential effect of macronutrient type and site of release on circulating concentrations of the L cell-derived enteroendocrine hormone peptide tyrosine tyrosine (amino acids 1 to 36) (PYY). Materials and Methods Eight healthy volunteers were recruited to a randomized, double-blinded, six-way crossover study. At each visit, the participants consumed a 500-kcal drink containing carbohydrate, protein, or fat in either gastric or small intestinal release formulations. Plasma PYY concentrations and hunger ratings were assessed for 3 hours after consumption of the test drink. The food intake was recorded thereafter at an ad libitum lunch. Results Microcapsular formulations targeting the distal small intestinal delivery of fat, but not carbohydrate or protein, markedly enhance PYY release relative to macronutrient delivery in gastric release formulations. Food intake at an ad libitum meal was lowest after consumption of the formulation releasing fat at the distal small intestine. Conclusion Targeting of fat to the distal small intestine in delayed release microcapsules enhanced PYY release and was associated with reductions in food intake.

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