scholarly journals Ghrelin secretion is not reduced by increased fat mass during diet-induced obesity

2008 ◽  
Vol 295 (2) ◽  
pp. R429-R435 ◽  
Author(s):  
Xiang Qi ◽  
Jason T. Reed ◽  
Guiyun Wang ◽  
Song Han ◽  
Ella W. Englander ◽  
...  
Keyword(s):  
Fat Mass ◽  
Caloric Intake ◽  
Inhibitory Effect ◽  
Ingestive Behavior ◽  
Sprague Dawley ◽  
Gh Secretion ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Chronic Ingestion ◽  
Ghrelin Secretion

Ghrelin is a stomach hormone that stimulates growth hormone (GH) secretion, adiposity, and food intake. Gastric ghrelin production and secretion are regulated by caloric intake; ghrelin secretion increases during fasting, decreases with refeeding, and is reduced by diet-induced obesity. The aim of the present study was to test the hypotheses that 1) an increase in body adiposity will play an inhibitory role in the reduction of gastric ghrelin synthesis and secretion during chronic ingestion of a high-fat (HF) diet and 2) chronic ingestion of an HF diet will suppress the rise in circulating ghrelin levels in response to acute fasting. Adult male Sprague-Dawley rats were fed a standard AIN-76A (∼5–12% of calories from fat) or an HF (∼45% of calories from fat) diet. The effect of increased adiposity on gastric ghrelin homeostasis was assessed by comparison of stomach ghrelin production and plasma ghrelin levels in obese and nonobese rats fed the HF diet. HF diet-fed, nonobese rats were generated by administration of triiodothyronine to lower body fat accumulation. Our findings indicate that an increased fat mass per se does not exert an inhibitory effect on ghrelin homeostasis during ingestion of the HF diet. Additionally, the magnitude of change in plasma ghrelin in response to fasting was not blunted, indicating that a presumed, endogenous signal for activation of ingestive behavior remains intact, despite excess stored calories in HF-fed rats.

Ontogeny of diet-induced obesity in selectively bred Sprague-Dawley rats

2003 ◽  
Vol 285 (3) ◽  
pp. R610-R618 ◽  
Author(s):  
Matthew R. Ricci ◽  
Barry E. Levin
Keyword(s):  
Leptin Receptor ◽  
Splice Variants ◽  
Caloric Intake ◽  
High Energy ◽  
Sprague Dawley ◽  
Low Fat Diet ◽  
Diet Induced Obesity ◽  
Leptin Sensitivity ◽  
Sprague Dawley Rats ◽  
Plasma Leptin

Outbred Sprague-Dawley rats selectively bred for their propensity to develop diet-induced obesity (DIO) become heavier on low-fat diet than those bred to be diet resistant (DR) beginning at ∼5 wk of age. Here we assessed the development of metabolic and neural functions for insights into the origins of their greater weight gain. From week 5 to week 10, chow-fed DIO rats gained 15% more body weight and ate ∼14% more calories but had only slightly greater adiposity and plasma leptin than DR rats. From day 3 through week 10, DIO and DR rats had similar mRNA expression of arcuate nucleus neuropeptide Y, proopiomelanocortin, agouti-related peptide, and all splice variants of the leptin receptor (OB-R). When fed a high-energy (HE; 31% fat) diet, 7-wk-old DIO rats had a 240% increase in plasma leptin levels after only 3 days. Despite this early leptin rise, they maintained a persistent hyperphagia and became more obese than chow-fed DIO rats and DR rats fed chow or HE diet. Their failure to reduce caloric intake, despite high levels of leptin, suggests that selectively bred DIO rats might have reduced leptin sensitivity similar to that seen in the outbred DIO parent strain.

Relationship between sympathetic activity and diet-induced obesity in two rat strains

1983 ◽  
Vol 245 (3) ◽  
pp. R364-R371 ◽  
Author(s):  
B. E. Levin ◽  
J. Triscari ◽  
A. C. Sullivan
Keyword(s):  
Sympathetic Activity ◽  
Caloric Intake ◽  
Sprague Dawley ◽  
Rat Strains ◽  
Sympathetic Function ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Calorie Diet ◽  
High Calorie Diet ◽  
High Calorie

Chronic diet-induced obesity developed in 50-60% of male Sprague-Dawley rats fed a relatively high-calorie diet for 90 days. The remaining rats decreased their caloric intake and resisted the development of obesity. All male Fischer F-344 rats fed this diet for 85 days became obese but to only half the degree of the obese Sprague-Dawley rats. The development of chronic obesity in both rat strains was associated with decreased norepinephrine (NE) levels in hearts and aortas and decreased NE turnover in aortas compared with chow-fed controls. However, 40-50% of the Sprague-Dawley rats did not become obese on this diet, yet showed similar findings suggesting an effect of dietary composition on sympathetic function. The more profoundly obese Sprague-Dawley rats additionally showed decreased or absent NE turnover in their hearts and pancreases. Since sympathetic function in both strains of rats with diet-induced obesity was either depressed or normal, it appears unlikely that the initial enhancement of sympathetic activity seen during short-term overfeeding plays an important continuing role in combating more chronic states of obesity in the rat.

Glucose-induced norepinephrine levels and obesity resistance

1987 ◽  
Vol 253 (3) ◽  
pp. R475-R481 ◽  
Author(s):  
B. E. Levin ◽  
A. C. Sullivan
Keyword(s):  
Weight Gain ◽  
Caloric Intake ◽  
Sympathetic Activation ◽  
Glucose Load ◽  
Sprague Dawley ◽  
Intravenous Glucose ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Calorie Diet ◽  
High Calorie

The value of glucose-stimulated sympathetic activation in differentiating rats that would subsequently resist or develop diet-induced obesity (DIO) when chronically fed a high-calorie diet (CM) enriched in fat and sucrose was tested in 3-mo-old male Sprague-Dawley rats. While the rats were on chow the areas under the curve for plasma glucose, insulin, and norepinephrine (NE) levels were measured for 60 min after an intravenous glucose load (1 g/kg). Half of the rats then switched to the CM diet for 14 wk developed DIO with 54% more weight gain and 205% heavier retroperitoneal fat pads; half [diet resistant (DR)] had weight gain and pad weights comparable to chow-fed controls. Caloric intake was comparable in all animals. NE areas after intravenous glucose loads were 54% lower in DR than DIO rats, and there was a positive correlation (r = 0.63) between these NE areas and subsequent weight gain on the CM diet. Areas under the insulin curve correlated with subsequent weight gain on chow (r = 0.71) but not the CM diet. These results suggest that rats predisposed to become DR on the CM diet have dampened sympathetic activation after a glucose load, possibly because of heightened end-organ responsiveness to NE.

Plasma growth hormone secretion is impaired in obesity-prone rats before onset of diet-induced obesity

1998 ◽  
Vol 275 (1) ◽  
pp. E6-E11 ◽  
Author(s):  
Thomas J. Lauterio ◽  
Ariel Barkan ◽  
Mark DeAngelo ◽  
Roberta DeMott-Friberg ◽  
Ray Ramirez
Keyword(s):  
Growth Hormone ◽  
Body Weight Gain ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Peak Height ◽  
Sprague Dawley ◽  
Concentration Difference ◽  
Gh Secretion ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats

Sprague-Dawley rats, which become obese (obesity prone) when fed a moderately high-fat (MHF; 32.5% of kcal as fat) diet, have decreased growth hormone (GH) concentrations compared with obesity-resistant rats fed the same diet. To determine whether plasma GH concentrations are different in obesity-prone rats compared with obesity-resistant rats before diet-induced obesity occurs, total integrated GH concentrations were determined in male Sprague-Dawley rats before exposure to the MHF diet. After initial blood sampling, rats were fed an MHF diet for 15 wk, over which time the animals were separated into two discrete populations based on body weight gain. Analysis of GH in episodic blood samples showed that the obesity-prone group had a GH secretion deficit before the onset of obesity (115.2 ± 12.9 ng ⋅ ml−1 ⋅ 200 min−1) compared with obesity-resistant rats (237.2 ± 47.1 ng ⋅ ml−1 ⋅ 200 min−1). The GH concentration difference was due to a decrease in mean GH peak height in rats that later became obese (34.8 ng/ml) compared with rats that remained lean (74.2 ng/ml). The results suggest that GH secretion impairment exists before dietary challenge or onset of obesity and may contribute to the susceptibility to obesity observed in these animals.

Defense of differfing body weight set points in diet-induced obese and resistant rats

1998 ◽  
Vol 274 (2) ◽  
pp. R412-R419 ◽  
Author(s):  
Barry E. Levin ◽  
Richard E. Keesey
Keyword(s):  
Body Weight ◽  
Diet Composition ◽  
Energy Homeostasis ◽  
Energy Content ◽  
Sprague Dawley ◽  
Fat Pad ◽  
Insulin Levels ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Plasma Leptin

Among outbred Sprague-Dawley rats, approximately one-half develop diet-induced obesity (DIO) and one-half are diet resistant (DR) on a diet relatively high in fat and energy content (HE diet). Here we examined the defense of body weight in these two phenotypes. After HE diet for 13 wk, followed by chow for 6 wk, DR rats gained weight comparably but their plasma leptin levels fell to 54% of chow-fed controls. When a palatable liquid diet (Ensure) was added for 13 wk, other DR rats became obese. But when switched to chow, their intakes fell by 60%, and body and retroperitoneal (RP) fat pad weights and plasma leptin and insulin levels all declined for 2 wk and then stabilized at control levels after 6 wk. In contrast, comparably obese DIO rats decreased their intake by only 20%, and their weights plateaued when they were switched to chow after 13 wk on HE diet. When a subgroup of these DIO rats was restricted to 60% of prior intake, their weights fell to chow-fed control levels over 2 wk. But their leptin and insulin levels both fell disproportionately to 30% of controls. When no longer restricted, their intake and feed efficiency rose immediately, and their body and RP pad weights and leptin and insulin levels rose to those of unrestricted DIO rats within 2 wk. Thus diet and genetic background interact to establish high (DIO) or low (DR) body weight set points, which are then defended against subsequent changes in diet composition and/or energy availability. If leptin affects energy homeostasis, it does so differentially in DIO vs. DR rats since comparably low and high levels were associated with differing patterns of weight change between the two phenotypes.

Specific inhibitory effect of dietary eicosapentaenoic acid on N-nitroso-N-methylurea-induced mammary carcinogenesis in female Sprague—Dawley rats

1990 ◽  
Vol 11 (11) ◽  
pp. 2015-2019 ◽  
Author(s):  
Toshiyuki Takata ◽  
Toshiyuki Minoura ◽  
Hideho Takada ◽  
Michitomo Sakaguchi ◽  
Manabu Yamamura ◽  
...  
Keyword(s):  
Eicosapentaenoic Acid ◽  
Mammary Carcinogenesis ◽  
Inhibitory Effect ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

scholarly journals Antiobesity Activity of Elateriospermum tapos Shell Extract in Obesity-Induced Sprague Dawley Rats

Molecules ◽  
2021 ◽  
Vol 26 (2) ◽  
pp. 321
Author(s):  
Kokila Vani Perumal ◽  
Nor Liyana Ja’afar ◽  
Che Norma Mat Taib ◽  
Nurul Husna Shafie ◽  
Hasnah Bahari
Keyword(s):  
Body Weight ◽  
Corn Starch ◽  
Milk Powder ◽  
Caloric Intake ◽  
Lipid Lowering ◽  
Sprague Dawley ◽  
Triglyceride Accumulation ◽  
Sprague Dawley Rats ◽  
Effective Result ◽  
Lipid Lowering Effect

Obesity is one of the risk factors associated with cardiovascular diseases, hypertension, abnormal liver function, diabetes, and cancers. Orlistat is currently available to treat obesity, but it is associated with adverse side effects. Natural resources are widely used for obesity treatment. Hence, this study aimed to investigate the anti-obesity activity of Elateriospermum tapos (E. tapos) shell extract in obesity induced Sprague Dawley rats. The rats’ obesity was induced by a high-fat (HF) diet made up of 50% standard rat pellet, 20% milk powder, 6% corn starch, and 24% ghee and a cafeteria (CAF) diet such as chicken rolls, salty biscuits, cakes, and cheese snacks. A hot aqueous method for the extraction of E. tapos shells was applied by using 500 mL of distilled water for about 24 h. Various dosages of E. tapos shell extract (10 mg/kg, 100 mg/kg, and 200 mg/kg) were used. At the end of the study, body weight, caloric intake, organ weight, lipid profile, lipoprotein lipase (LPL) activity, and histopathology analysis were carried out. E. tapos shell extract treated groups showed a reduction in body weight, positive lipid-lowering effect, decrements in triglyceride accumulation and LPL activity, and positive improvement in histopathology analysis. A dose of 200 mg/kg showed the most effective result compared to 10 mg/kg and 100 mg/kg doses.

Effect of sodium fluoride on concentrating and diluting ability in the rat

1977 ◽  
Vol 232 (4) ◽  
pp. F335-F340 ◽  
Author(s):  
J. D. Wallin ◽  
R. A. Kaplan
Keyword(s):  
Cyclic Amp ◽  
Urine Volume ◽  
Free Water ◽  
Urine Osmolality ◽  
Inhibitory Effect ◽  
Sprague Dawley ◽  
Free Water Clearance ◽  
Sprague Dawley Rats ◽  
Direct Inhibitory Effect ◽  
Hereditary Hypothalamic Diabetes Insipidus

Mechanisms for the concentrating defect produced by fluoride were examined in the rat. Free-water clearance at all levels of delivery was normal after 5 days of chronic fluoride administration in the hereditary hypothalamic diabetes insipidus rat. In the Sprague-Dawley rats, during moderate fluoride administration (120 micronmol/kg per day), urine osmolality and cyclic AMP excretion decreased and urine volume increased, but after exogenous vasopressin, volume decreased and osmolality and cyclic AMP increased appropriately. During larger daily doses of fluoride (240 micronmol/kg per day) urinary osmolality and cyclic AMP decreased and volume increased, which was similar to the changes seen during lower fluoride dosages, but these parameters did not change after exogenous vasopressin. These data suggest that ascending limb chloride reabsorption is unaltered by fluoride administration; in the presence of sufficient fluoride, collecting tubular cells apparently do not generate cyclic AMP or increase permeability appropriately in response to vasopressin. The postulated defect is felt to be due to either a decrease in ATP availability or to a direct inhibitory effect of fluoride on the vasopressin-dependent cyclic AMP generating system.

Brown adipose and metabolic features of chronic diet-induced obesity

1985 ◽  
Vol 248 (6) ◽  
pp. R717-R723 ◽  
Author(s):  
B. E. Levin ◽  
M. Finnegan ◽  
J. Triscari ◽  
A. C. Sullivan
Keyword(s):  
Metabolic Efficiency ◽  
Sprague Dawley ◽  
High Fat ◽  
Interscapular Brown Adipose Tissue ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Norepinephrine Turnover ◽  
Brown Adipose ◽  
Plasma Insulin Levels

Half of the 3-mo male Sprague-Dawley rats fed a high-fat (DIO) diet for 5 mo became obese and had increased carcass lipid (106%) and plasma insulin levels (61%), despite 8% less total energy intake than chow-fed controls. Their interscapular brown adipose tissue (IBAT) was 52% heavier with 45% more lipid and larger uni- and multilocular cells. Norepinephrine turnover was normal in their hearts, pancreases, and aortas but undetectable in IBAT where in vitro lipolysis, but not O2 consumption (VO2), was enhanced. Half the rats fed the DIO diet ate 17% fewer calories, gained weight equally to controls, but still had 34% more carcass lipid. Their IBAT was heavier, contained 103% more protein, with no detectable norepinephrine turnover, whereas maximal lipolysis was 73% lower and maximal VO2 was the same or even lower than controls. IBAT VO2 was stimulated by switching 8-mo chow-fed controls to the DIO diet for 7 days (which caused a 480% greater weight gain) but not by switching 8-mo obese rats to chow for 3 days. Therefore metabolic efficiency was increased while BAT VO2 and norepinephrine turnover were unchanged or reduced compared with controls by either chronic obesity or a high-fat diet.

scholarly journals Effects of Melatonin on Lipid Metabolism and Circulating Irisin in Sprague-Dawley Rats with Diet-Induced Obesity

Molecules ◽  
2020 ◽  
Vol 25 (15) ◽  
pp. 3329
Author(s):  
Yu-Tang Tung ◽  
Pei-Chin Chiang ◽  
Ya-Ling Chen ◽  
Yi-Wen Chien
Keyword(s):  
Weight Gain ◽  
Total Cholesterol ◽  
Vehicle Control ◽  
Serum Total Cholesterol ◽  
Sprague Dawley ◽  
High Fat ◽  
Melatonin Treatment ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Cholesterol Excretion

Melatonin, a pivotal photoperiodic signal transducer, may work as a brown-fat inducer that regulates energy balance. Our study aimed to investigate the effects of melatonin treatment on the body fat accumulation, lipid profiles, and circulating irisin of rats with high-fat diet-induced obesity (DIO). Methods: 30 male Sprague-Dawley rats were divided into five groups and treated for 8 weeks: vehicle control (VC), positive control (PC), MEL10 (10 mg melatonin/kg body weight (BW)), MEL20 (20 mg/kg BW), and MEL50 (50 mg/kg BW). The vehicle control group was fed a control diet, and the other groups were fed a high-fat and high-calorie diet for 8 weeks to induce obesity before the melatonin treatment began. Melatonin reduced weight gain without affecting the food intake, reduced the serum total cholesterol level, enhanced the fecal cholesterol excretion, and increased the circulating irisin level. Melatonin downregulated the fibronectin type III domain containing 5 (FNDC5) and lipoprotein lipase (LPL) mRNA expressions of inguinal white adipose tissue (iWAT) and induced the browning of iWAT in both the MEL10 and MEL20 groups. Conclusion: Chronic continuous melatonin administration in drinking water reduced weight gain and the serum total cholesterol levels. Additionally, it enhanced the circulating irisin, which promoted brite/beige adipocyte recruitment together with cholesterol excretion and contributed to an anti-obesity effect.

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