scholarly journals Improved gastric emptying in diabetic rats by irbesartan via decreased serum leptin and ameliorated gastric microcirculation

2014 ◽  
Vol 13 (3) ◽  
pp. 7163-7172 ◽  
Author(s):  
L. He ◽  
Y. Sun ◽  
Y. Zhu ◽  
R. Ren ◽  
Y. Zhang ◽  
...  
1984 ◽  
Vol 247 (6) ◽  
pp. R1054-R1061 ◽  
Author(s):  
J. G. Granneman ◽  
E. M. Stricker

Recent studies suggest that the rate of nutrient transit through the upper gastrointestract may provide cues that are important to the control of food intake. We examined gastrointestinal function in rats with streptozotocin-induced diabetes and related these findings to concomitant changes in food intake. Control and diabetic rats were adapted to one of two isocaloric diets either high in carbohydrate or fat. Control rats ate similar amounts of each diet. In contrast, diabetic animals fed high-carbohydrate diet were hyperphagic, whereas those fed low-carbohydrate diet ate normal amounts of food. Gastric emptying, intestinal mass, disaccharidase activity, and glucose absorption were increased in normophagic diabetic rats fed a low-carbohydrate diet. Feeding diabetic rats high-carbohydrate diet potentiated each of these effects, and food intake was highly correlated with rate of gastric emptying. These and other results indicate that diabetes enhances gastric emptying and intestinal carbohydrate digestion and absorption, even in the absence of hyperphagia. Consequently, the hyperphagia of diabetic rats may be in part a behavioral response to a greatly accelerated clearance of nutrients from the upper gastrointestinal tract that occurs when these animals are fed diets rich in carbohydrate.


2017 ◽  
Vol 40 (9) ◽  
pp. 1506-1514 ◽  
Author(s):  
Nipaporn Muangchan ◽  
Suwattanee Kooptiwut ◽  
Sompol Tapechum ◽  
Pravit Akarasereenont ◽  
Nuanchan Vongsopanagul ◽  
...  

2012 ◽  
Vol 514 (1) ◽  
pp. 77-81 ◽  
Author(s):  
Hajime Ariga ◽  
Kenji Imai ◽  
Kirk Ludwig ◽  
Toku Takahashi

Endocrinology ◽  
2007 ◽  
Vol 149 (2) ◽  
pp. 445-454 ◽  
Author(s):  
Sunmin Park ◽  
Sang Mee Hong ◽  
So Ra Sung ◽  
Hye Kyung Jung

To determine the long-term effect of central leptin and resistin on energy homeostasis, peripheral insulin resistance, and β-cell function and mass, intracerebroventricular (ICV) infusion of leptin (3 ng/h), resistin (80 ng/h), leptin plus resistin, and cerebrospinal fluid (control) was conducted by means of an osmotic pump for 4 wk on normal rats and 90% pancreatectomized diabetic rats fed 40% fat-energy diets. Overall, the effects were greater in diabetic rats than normal rats. Leptin infusion, causing a significant reduction in food intake, decreased body weight and epididymal fat. However, resistin and leptin plus resistin reduced epididymal fat with decreased serum leptin levels in comparison with the control. Unlike serum leptin, only resistin infusion lowered serum resistin levels. Central leptin increased glucose infusion rates during euglycemic hyperinsulinemic clamp and suppressed hepatic glucose production in the hyperinsulinemic state in comparison with the control. However, central leptin did not affect glucose-stimulated insulin secretion and β-cell mass. Central resistin infusion also increased peripheral insulin sensitivity, but not as much as leptin. Unlike leptin, resistin significantly increased first-phase insulin secretion during hyperglycemic clamp and β-cell mass by augmenting β-cell proliferation. These metabolic changes were associated with hypothalamic leptin and insulin signaling. ICV infusion of leptin potentiated signal transducer and activator of transcription 3 phosphorylation and attenuated AMP kinase in the hypothalamus, but resistin had less potent effects than leptin. Leptin enhanced insulin signaling by potentiating IRS2→Akt pathways, whereas resistin activated Akt without augmenting insulin receptor substrate 2 phosphorylation. In conclusion, long-term ICV infusion of leptin and resistin independently improved energy and glucose homeostasis by modulating in different ways hypothalamic leptin and insulin signaling.


BMC Surgery ◽  
2002 ◽  
Vol 2 (1) ◽  
Author(s):  
Isabelle Le Blanc-Louvry ◽  
Florence Guerre ◽  
Badjona Songné ◽  
Philippe Ducrotté

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Hamideh Dinari Ghozhdi ◽  
Ali Heidarianpour ◽  
Maryam Keshvari ◽  
Hassan Tavassoli

Abstract Background Adipocytokines, which are secreted by the adipose tissue, contribute to the pathogenesis of obesity-related complications. To evaluate this assumption, we investigated the effects of aerobic exercise training (AET), resistance exercise training (RET), and 4 weeks of de-training on serum leptin and TNF-α levels in diabetic rats. Method 36 Wistar rats were divided into normal diet (ND) (control, RET, AET) and high-fat diet (HFD) + STZ (control, RET, AET) groups. Serum insulin, leptin, and TNF-α levels were assessed by commercial ELISA kits. Also fasting blood glucose (FBG), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) levels were measured by the colorimetric kits. Results Diabetes induction increased body weight (BW) and FBG, and decreased insulin compared to the ND rats’ groups (p < 0.001). 12-weeks of AET and RET programs in the trained diabetic rats led to a decrease in TG, LDL-C, leptin, TNF-α, and FBG, and an increase in insulin compared to the HFD + STZ-C group (p < 0.001). Besides, there was no difference between AET and RET in improving the variables studied (p > 0.05). Also, de-training led to increased BW, TG, leptin, and TNF-α compared to the end of the exercise training (p < 0.05). The correlation between the variables studied was established at different stages of the study (p < 0.05), and only BW was not correlated with insulin during exercise training and de-training (p > 0.05). Conclusion These findings indicate that both AET and RET are useful in reducing levels of serum adipocytokines (TNF-α, leptin) in diabetic and non-diabetic rats. At the same time, 4 weeks of de-training was sufficient to lose the metabolic adaptations.


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