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 ◽  
...  
Diabetes ◽  
1989 ◽  
Vol 38 (2) ◽  
pp. 219-224 ◽  
Author(s):  
K. R. Feingold ◽  
Q.-H. Zeng ◽  
M. Soued ◽  
A. Siperstein ◽  
M. K. Serio ◽  
...  

1984 ◽  
Vol 247 (5) ◽  
pp. G494-G501
Author(s):  
K. R. Feingold ◽  
A. H. Moser

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.


1997 ◽  
Vol 273 (4) ◽  
pp. E815-E820 ◽  
Author(s):  
Kirk D. Fischer ◽  
Savita Dhanvantari ◽  
Daniel J. Drucker ◽  
Patricia L. Brubaker

Glucagon-like peptide 2 (GLP-2) has recently been identified as a novel intestinal growth factor. Because experimental diabetes is associated with bowel growth, we examined the relationship between GLP-2 and intestinal growth in rats made diabetic by streptozotocin (STZ) injection and treated with or without insulin for 3 wk. Ileal concentrations of the intestinal proglucagon-derived peptides, i.e., glicentin + oxyntomodulin, and GLPs 1 and 2, were increased by 57 ± 20% above those of controls in untreated STZ diabetes ( P < 0.05–0.001). Similar increases in plasma concentrations of glicentin + oxyntomodulin (77 ± 15% above controls, P < 0.01) and GLP-2 (91 ± 32% above controls, P < 0.05) were seen in untreated STZ diabetes. Both wet and dry small intestinal weight increased by 74 ± 20% above controls ( P < 0.01) in STZ diabetes, and macromolecular analysis indicated parallel increases in both protein ( P < 0.001) and lipid ( P < 0.05) content. Villus height ( P < 0.001) and crypt depth ( P < 0.01) were also increased in untreated diabetic rat intestine. Insulin therapy prevented the changes in plasma GLP-2 and intestinal mass seen in untreated STZ diabetes. Thus STZ diabetes is associated with both increased production of GLP-2 and enhanced bowel weight, thereby suggesting a role for GLP-2 in diabetes-associated bowel growth.


1986 ◽  
Vol 251 (3) ◽  
pp. G362-G369
Author(s):  
K. R. Feingold ◽  
G. Zsigmond ◽  
S. R. Lear ◽  
A. H. Moser

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)


2010 ◽  
Vol 298 (4) ◽  
pp. G563-G570 ◽  
Author(s):  
Jieyun Yin ◽  
Jie Chen ◽  
Jiande D. Z. Chen

The aim of this study was to investigate the effects and mechanisms of electroacupuncture (EA) on gastric accommodation, gastric dysrhythmia, and gastric emptying (GE) in streptozotocin (STZ)-induced diabetic rats. Five experiments were performed in five groups of STZ-induced diabetic rats to study the effects of EA at ST-36 (Zusanli) on gastric slow-wave dysrhythmia, delayed GE and intestinal transit, impaired gastric accommodation, and the mechanisms of EA involving the autonomic and opioidergic pathways. We found the following: 1) EA improved gastric dysrhythmia in the diabetic rats. The normal percentage of slow waves was 55.4 ± 2.9% at baseline and significantly increased to 69.2 ± 2.2% with EA ( P = 0.01); this effect was blocked by naloxone. 2) EA resulted in a 21.4% increase in GE and 18.2% increase in small intestinal transit in the diabetic rats. 3) EA restored diabetes-induced impairment in gastric accommodation. Gastric accommodation was 0.98 ± 0.13 ml with sham EA and significantly increased to 1.21 ± 0.15 ml with EA ( P = 0.01), and this effect was blocked by naloxone. 4) EA increased vagal activity assessed by the spectral analysis of the heart rate variability. We concluded that EA at ST-36 improves gastric dysrhythmia, delayed GE and intestinal transit, and impaired accommodation in STZ-induced diabetic rats, and the improvement seems to be mainly mediated via the vagal pathway. EA may have a promising therapeutic potential for diabetic gastroparesis.


1974 ◽  
Vol 20 (1) ◽  
pp. 71-79
Author(s):  
Yukihiro NAKABOU ◽  
Mayumi FUJIMOTO ◽  
Chiyo OKITA ◽  
Yasuo TAKANO ◽  
Hiroshi HAGIHIRA

1985 ◽  
Vol 249 (5) ◽  
pp. G634-G641 ◽  
Author(s):  
K. R. Feingold ◽  
A. H. Moser

Previous studies have demonstrated that cholesterol synthesis is increased twofold in the small intestines of rats with streptozotocin-induced diabetes. The purpose of the present study was to determine the effect of adding glucose or fructose to standard rat chow on cholesterol synthesis in control and diabetic rats. In control rats a 25% glucose or fructose diet fed for 21 days markedly inhibited hepatic cholesterol synthesis in the liver. In contrast, in diabetic animals only fructose inhibited hepatic cholesterol synthesis. In both control and diabetic animals the addition of these simple sugars to the diet did not markedly alter extrahepatic cholesterol synthesis. The enhancement of small intestinal cholesterol synthesis observed in diabetic animals was present regardless of the dietary manipulations. Further studies demonstrated that the addition of smaller concentrations of fructose (10%) to standard rat chow decreased hepatic cholesterol synthesis in both control and diabetic rats. Similarly the addition of fructose to the diet of control and diabetics for a period as short as 2 days was also sufficient to inhibit hepatic cholesterol synthesis. In both control and diabetic animals, fructose feeding decreased hepatic 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase activity but did not alter the percentage of HMG-CoA reductase in the active form. Finally, the intestinal hypertrophy and stimulation of intestinal cholesterogenesis that are characteristic of streptozotocin-induced diabetes occurred when either glucose or fructose was the sole caloric source.


1960 ◽  
Vol 198 (1) ◽  
pp. 25-28 ◽  
Author(s):  
Daniel W. Foster ◽  
Marvin D. Siperstein

The synthesis of cholesterol and fatty acids from acetate-1-C14 was studied in the aortas and livers of 42 diabetic rats and their normal controls. Hepatic cholesterol synthesis was significantly increased in 13, decreased in 13, and unchanged in 16 of the 42 animals. Fatty acid synthesis was depressed in the liver in 39 of the 42 diabetic rats. Aortic cholesterogenesis was increased in only 2 of the 13 aortas from the same rats showing elevated hepatic cholesterol synthesis. Fatty acid synthesis was depressed in 21 of 42 aortas from the diabetic group. It is concluded, therefore, that the aorta is relatively resistant to stimulation of cholesterol synthesis by diabetes even when hepatic cholesterol synthesis in the same animal is elevated. Lipogenesis on the other hand is commonly depressed in the aorta as well as the liver. Cholesterol was purified through dibrominization and both normal and diabetic aortas were shown to be capable of carrying cholesterol synthesis to completion.


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