Subdiaphragmatic vagal deafferentation affects body weight gain and glucose metabolism in obese male Zucker (fa/fa) rats

2005 ◽  
Vol 289 (4) ◽  
pp. R1027-R1034 ◽  
Author(s):  
Bettina Ferrari ◽  
Myrtha Arnold ◽  
Richard D. Carr ◽  
Wolfgang Langhans ◽  
Giovanni Pacini ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Food Intake ◽  
Plasma Glucose ◽  
Body Weight Gain ◽  
Zucker Rats ◽  
Sensitivity Index ◽  
Insulin Sensitivity Index ◽  
Obese Rats

We investigated the effect of subdiaphragmatic vagal deafferentation (SDA) on food intake, body weight gain, and metabolism in obese ( fa/ fa) and lean ( Fa/?) Zucker rats. Before and after recovery from surgery, food intake and body weight gain were recorded, and plasma glucose and insulin were measured in tail-prick blood samples. After implantation of a jugular vein catheter, an intravenous glucose tolerance test (IVGTT) was performed, followed by minimal modeling to estimate the insulin sensitivity index. Food intake relative to metabolic body weight (g/kg0.75) and daily body weight gain after surgery were lower ( P < 0.05) in SDA than in sham obese but not lean rats. Before surgery, plasma glucose and insulin concentrations were lower ( P < 0.05) in lean than in obese rats but did not differ between surgical groups within both genotypes. Four weeks after surgery, plasma glucose and insulin were still similar in SDA and sham lean rats but lower ( P < 0.05) in SDA than in sham obese rats. IVGTT revealed a downward shift of the plasma insulin profile by SDA in obese but not lean rats, whereas the plasma glucose profile was unaffected. SDA decreased ( P < 0.05) area under the curve for insulin but not glucose in obese rats. The insulin sensitivity index was higher in lean than in obese rats but was not affected by SDA in both genotypes. These results suggest that elimination of vagal afferent signals from the upper gut reduces food intake and body weight gain without affecting the insulin sensitivity index measured by minimal modeling in obese Zucker rats.

987 des-acyl Ghrelin Suppresses Food Intake and Body Weight Gain in Adult Obese Zucker Rats

2008 ◽  
Vol 134 (4) ◽  
pp. A-148 ◽  
Author(s):  
Andreas Stengel ◽  
Anna-Sophia Wisser ◽  
Peter Kobelt ◽  
Miriam Goebel ◽  
Bertram Wiedenmann ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Zucker Rats ◽  
Obese Zucker Rats ◽  
Acyl Ghrelin

LY226936 Administered Orally and Centrally to Obese Zucker Rats Suppresses Food Intake and Body Weight Gain

1994 ◽  
Vol 2 (5) ◽  
pp. 458-468
Author(s):  
Walter N. Shaw ◽  
James A. Clemens ◽  
Jill A. Parietta
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Zucker Rats ◽  
Obese Zucker Rats

Effect of phenoxybenzamine on development of adipose tissue in lean and obese Zucker rats

1982 ◽  
Vol 243 (5) ◽  
pp. E398-E406
Author(s):  
K. Comai ◽  
A. C. Sullivan
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Cell Size ◽  
Body Weight Gain ◽  
Zucker Rats ◽  
Fat Cell ◽  
Fat Depots ◽  
Fat Cell Size ◽  
Obese Rats ◽  
Fat Depot

Young male Zucker lean (Fa/-) and obese (fa/fa) rats were fed the alpha-adrenergic blocking agent phenoxybenzamine as a dietary admixture for 35 days. In lean and obese rats, phenoxybenzamine treatment decreased significantly body weight gain, food consumption, grams of carcass fat, and grams of carcass protein. Lean rats exhibited reduced fat cell size and number in retroperitoneal, epididymal, and inguinal fat depots. Obese rats treated with phenoxybenzamine exhibited significantly decreased numbers of fat cells in the retroperitoneal, epididymal, and inguinal fat depots and a small decreased cell size in the inguinal fat depot only. The levels of carcass fat and protein and fat cell number in obese and lean rats treated with phenoxybenzamine for 35 days were similar to pretreatment values in agreement with the lack of body weight gain. Although values in agreement with the lack of body weight gain. Although rats exhibited marked decreases in fat accumulation during phenoxybenzamine treatment, fat cell size and number returned to control values during the posttreatment period with a marked hyperplasia occurring particularly in the retroperitoneal fat depot of obese rats. Serum levels of insulin were suppressed and free fatty acid levels increased in obese rats during phenoxybenzamine treatment, suggesting a stimulation of the sympathoadrenal system. This study shows that despite severe restrictions in fat cell proliferation during the rapid-growth phase of the obese Zucker rat, the mechanisms for cellular proliferation and fat deposition remain intact.

scholarly journals Pasta supplemented with isolated lupin protein fractions reduces body weight gain and food intake of rats and decreases plasma glucose concentration upon glucose overload trial

2014 ◽  
Vol 5 (2) ◽  
pp. 375-380 ◽  
Author(s):  
Jessica Capraro ◽  
Chiara Magni ◽  
Alessio Scarafoni ◽  
Rosita Caramanico ◽  
Filippo Rossi ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Plasma Glucose ◽  
Body Weight Gain ◽  
Seed Proteins ◽  
Well Being ◽  
Biologically Active ◽  
Lupin Protein ◽  
Powerful Approach

The supplementation of foods with biologically active seed proteins can be a powerful approach for controlling body weight gain and glycaemia, thus improving well being.

S 23521 Decreases Food Intake and Body Weight Gain in Diet-Induced Obese Rats

2004 ◽  
Vol 12 (10) ◽  
pp. 1596-1603 ◽  
Author(s):  
Marc Claret ◽  
Helena Corominola ◽  
Ignasi Canals ◽  
Belén Nadal ◽  
Alain Chavanieu ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Obese Rats

scholarly journals Chronic injection of pansomatostatin agonist ODT8-SST differentially modulates food intake and decreases body weight gain in lean and diet-induced obese rats

2011 ◽  
Vol 167 (2-3) ◽  
pp. 201-208 ◽  
Author(s):  
Andreas Stengel ◽  
Tamer Coskun ◽  
Miriam Goebel-Stengel ◽  
Libbey S. Craft ◽  
Jorge Alsina-Fernandez ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Obese Rats ◽  
Chronic Injection

Food intake controls in the suckling pig: glucoprivation and gastrointestinal factors.

1977 ◽  
Vol 232 (5) ◽  
pp. E510
Author(s):  
K A Houpt ◽  
T R Houpt ◽  
W G Pond
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Energy Balance ◽  
Food Intake ◽  
Food Deprivation ◽  
Plasma Glucose ◽  
Corn Oil ◽  
Protein Hydrolysate ◽  
Body Weight Gain ◽  
Yorkshire Pigs

The energy balance of suckling Yorkshire pigs 1 day to 2 wk old was challenged by: food deprivation, glucoprivation, and caloric and noncaloric gastric loads delivered by intubation. tafter 2--4 h fasts, food intake greatly increased over nonfasted control intake during a 3-h refeeding period. This response occurred both when body weight gain was used as a measure of intake for pigs nursing on the sow and when intake was measured directly in bottle-fed pigs. Glucoprivation produced by 0.5--2 U/kg insulin did not stimulate food intake although plasma glucose fell to a mean of 49 mg/100 ml (43% of control) after 1 U/kg insulin. Gastric loads of water or 3% NACl depressed intake after 3-h fast, but 0.9% NaCl did not. All the caloric gastric loads depressed intake; in order of increasing effectiveness, they were: heavy cream, protein hydrolysate, corn oil, milk, 5% glucose, and 5% lactose. The carbohydrate loads were most effective, a result which indicates that the response was not to calories alone but to some specific nutrient, possibly glucose.

Influence of Thyroid Status on Body Weight Gain, Food Intake and Serum Lipid Levels in Genetically Obese Zucker Rats

1987 ◽  
Vol 117 (1) ◽  
pp. 159-163 ◽  
Author(s):  
Annie Loireau ◽  
Paul Dumas ◽  
Nicole Autissier ◽  
Raymond Michel
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Serum Lipid ◽  
Body Weight Gain ◽  
Zucker Rats ◽  
Lipid Levels ◽  
Thyroid Status ◽  
Serum Lipid Levels ◽  
Obese Zucker Rats

Improvement of mild hypoinsulinaemic diabetes in the rat by low non-toxic doses of vanadate

1994 ◽  
Vol 142 (3) ◽  
pp. 555-561 ◽  
Author(s):  
J C Henquin ◽  
F Carton ◽  
L N Ongemba ◽  
D J Becker
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Glucose Homeostasis ◽  
Plasma Glucose ◽  
Body Weight Gain ◽  
Oral Glucose ◽  
Low Doses ◽  
Glucose Levels ◽  
Vanadium Salts

Abstract To exert their anti-diabetic effects in animals with overt alterations of glucose homeostasis, vanadium salts must be administered in high doses, which also cause decreases in food intake and body weight gain. In this study, we evaluated the effect of low doses of vanadate in rats made mildly diabetic (fed plasma glucose levels ∼11 mmol/l) and moderately hypoinsulinaemic by the injection of streptozotocin 4 days after birth. Vanadate was added to food and drinking water, at concentrations that led to the consumption of about 1 mg vanadium element per day (∼2·65 mg vanadium/kg per day in adult rats), i.e. three to fivefold less than in previous studies. The treatment was started at weaning and lasted 22 weeks (V rats), or was administered for 9 weeks only from the age of 3 months (C-V rats). Food intake and body weight gain were not affected in V rats and decreased by no more than 10% in C-V rats. In V rats, fasted and fed plasma glucose levels were decreased by about 0·5 and 2–3 mmol/l, respectively. The rises in glycaemia after three oral glucose tolerance tests were also clearly attenuated. These effects were not accompanied by any changes in plasma insulin levels. Pancreatic insulin reserves (decreased by two-thirds as compared with normal rats) were not affected by the treatment. A decrease in plasma glucose levels was also noted in C-V rats, and this improvement disappeared upon cessation of the treatment. In conclusion, oral vanadate improves glucose homeostasis in rats with moderate insulin deficiency and diabetes, even when the element is administered at low doses which have practically no repercussions on food intake and body weight gain. This indicates that vanadium salts have genuine beneficial effects on glucose metabolism in vivo. Journal of Endocrinology (1994) 142, 555–561

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