The effect of metformin on food intake and its potential role in hypothalamic regulation in obese diabetic rats

2012 ◽  
Vol 1444 ◽  
pp. 11-19 ◽  
Author(s):  
Wen-shan Lv ◽  
Jun-ping Wen ◽  
Li Li ◽  
Rui-xia Sun ◽  
Jing Wang ◽  
...  
Keyword(s):  
Food Intake ◽  
Potential Role ◽  
Diabetic Rats ◽  
Hypothalamic Regulation ◽  
Obese Diabetic Rats

A PPARψ agonist improved diabetic state via decreasing TNF-α without any change including obesity in genetically obese diabetic rats

2001 ◽  
Vol 120 (5) ◽  
pp. A674-A674 ◽  
Author(s):  
A FUNAKOSHI ◽  
M ICHIKAWA ◽  
Y SATO ◽  
S KANAI ◽  
M OHTA ◽  
...  
Keyword(s):  
Diabetic Rats ◽  
Diabetic State ◽  
Tnf Α ◽  
Obese Diabetic Rats

The effect of phlorizin treatment on food intake and hypothalamic neuropeptide Y in normal and diabetic rats

1991 ◽  
Vol 35 (3) ◽  
pp. 227
Author(s):  
M Bose ◽  
J.P.H. Wilding ◽  
P.D. Lambert ◽  
N Aslam ◽  
M.A. Ghatei ◽  
...  
Keyword(s):  
Food Intake ◽  
Neuropeptide Y ◽  
Diabetic Rats

scholarly journals Hindbrain glucagon-like peptide-1 neurons track intake volume and contribute to injection stress-induced hypophagia in meal-entrained rats

2016 ◽  
Vol 310 (10) ◽  
pp. R906-R916 ◽  
Author(s):  
Alison D. Kreisler ◽  
Linda Rinaman
Keyword(s):  
Food Intake ◽  
Potential Role ◽  
Liquid Diet ◽  
Neural Activation ◽  
Intracerebroventricular Injection ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Diet Intake ◽  
Published Research ◽  
Diet Type

Published research supports a role for central glucagon-like peptide 1 (GLP-1) signaling in suppressing food intake in rodent species. However, it is unclear whether GLP-1 neurons track food intake and contribute to satiety, and/or whether GLP-1 signaling contributes to stress-induced hypophagia. To examine whether GLP-1 neurons track intake volume, rats were trained to consume liquid diet (LD) for 1 h daily until baseline intake stabilized. On test day, schedule-fed rats consumed unrestricted or limited volumes of LD or unrestricted volumes of diluted (calorically matched to LD) or undiluted Ensure. Rats were perfused after the test meal, and brains processed for immunolocalization of cFos and GLP-1. The large majority of GLP-1 neurons expressed cFos in rats that consumed satiating volumes, regardless of diet type, with GLP-1 activation proportional to intake volume. Since GLP-1 signaling may limit intake only when such large proportions of GLP-1 neurons are activated, a second experiment examined the effect of central GLP-1 receptor (R) antagonism on 2 h intake in schedule-fed rats. Compared with baseline, intracerebroventricular vehicle (saline) suppressed Ensure intake by ∼11%. Conversely, intracerebroventricular injection of vehicle containing GLP-1R antagonist increased intake by ∼14% compared with baseline, partly due to larger second meals. We conclude that GLP-1 neural activation effectively tracks liquid diet intake, that intracerebroventricular injection suppresses intake, and that central GLP-1 signaling contributes to this hypophagic effect. GLP-1 signaling also may contribute to satiety after large volumes have been consumed, but this potential role is difficult to separate from a role in the hypophagic response to intracerebroventricular injection.

TREADMILL EXERCISE TRAINING PROTECTS AGAINST METABOLIC DYSFUNCTION AND DIAPHRAGM WEAKNESS IN OBESE DIABETIC RATS

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Noriko Ichinoseki‐Sekine ◽  
Takamasa Tsuzuki ◽  
Matthew J. Hinkley ◽  
Toshinori Yoshihara ◽  
Hiroyuki Kobayashi ◽  
...  
Keyword(s):  
Exercise Training ◽  
Treadmill Exercise ◽  
Diabetic Rats ◽  
Metabolic Dysfunction ◽  
Obese Diabetic Rats ◽  
Diaphragm Weakness

scholarly journals Effect of canagliflozin or metformin on metabolic disorders in obese diabetic rats

2015 ◽  
Vol 9 (46) ◽  
pp. 1071-1079 ◽  
Author(s):  
S Marie Mohamed Assem ◽  
Mohamed Said Arafa Nadia ◽  
Abdullah Mubarak Alazimi Sara
Keyword(s):  
Metabolic Disorders ◽  
Diabetic Rats ◽  
Obese Diabetic Rats

Food intake and gastric emptying in rats with streptozotocin-induced diabetes

1984 ◽  
Vol 247 (6) ◽  
pp. R1054-R1061 ◽  
Author(s):  
J. G. Granneman ◽  
E. M. Stricker
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Glucose Absorption ◽  
Diabetic Rats ◽  
High Carbohydrate Diet ◽  
Carbohydrate Diet ◽  
Low Carbohydrate Diet ◽  
High Carbohydrate ◽  
Low Carbohydrate ◽  
Streptozotocin Induced Diabetes

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.

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