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

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.

1987 ◽  
Vol 253 (3) ◽  
pp. R475-R481 ◽  
Author(s):  
B. E. Levin ◽  
A. C. Sullivan

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.


Author(s):  
Haneen Jadir ◽  
Mohammed Jassim ◽  
Feryal Hussein

This study was designed to identify the effects of certain fat burners and functional foods on lipid profiles including total cholesterol (TC), triglycerides (TG), low-density lipoproteins (LDL-C), and antioxidants such as glutathione peroxidase (GPx) and malondialdehyde (MDA) in adult male Sprague–Dawley rats. The rats were separated into seven groups, each group containing six rats. Both the (T1) negative and (T2) positive control groups and the five other groups were fed with a high-calorie diet to achieve obesity. After the end of the feeding period, over 56 days the rats were treated with Orlistat 0.3mg/g (T3), C4 RIPPED 1.2 mg/g (T4), Garcinia Herb 0.5 mg/g (T5), Ispaghula Herb 0.02g/g (T6), and Functional Yoghurt 1ml (T7). The results showed significantly increased (p≤0.05) cholesterol in the serum of T2 rats compared with T1 rats. Transactions with T3, T4, T5, T6, and T7 rats led to a significant decrease in TC. There was a significant increase in TG and LDL-C in T2 rats compared with T1 rats; a significant decrease occurred in the serum of the animals treated in groups T3, T4, T5, T6, T7 and T7. Rats in groups T3, T5, T6, and T7 showed increased GPx and decreased MDA compared with T1 and T4.


2021 ◽  
Vol 11 (5) ◽  
pp. 123-133
Author(s):  
Alona Yurchenko ◽  
Daryna Krenytska ◽  
Olesya Kalmukova ◽  
Nataliia Raksha ◽  
Tetiana Halenova ◽  
...  

2003 ◽  
Vol 285 (3) ◽  
pp. R610-R618 ◽  
Author(s):  
Matthew R. Ricci ◽  
Barry E. Levin

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.


Author(s):  
Mokrani Zoulikha ◽  
Zerrouki Nacira ◽  
Gernigon-Spichalowicz Therese ◽  
Soltani Yacine

Abstract Objectives Who disrupts who? It is not clear what the interaction is between a high calorie diet (HCD) and adrenal axis activation in obesity. The goal was to assess the effect of two hypercaloric diets commercialized in Algeria on the hormonal and metabolic profile of the adrenal gland in rabbits. Methods Two classes of local male adult rabbits (n=16) and a finishing diet (FD) as a control for 15 weeks. Results It has been shown that HCD-received animals have developed visceral obesity, dyslipidemia and insulin resistance IR by dramatically increasing body weight, visceral fat tissue and adrenal weight, combined with elevated plasma levels of ACTH, cortisol, leptin and insulin. The HCD diet increased the levels of cortisol in the visceral adipose tissue (VAT), in peri-adrenal adipose tissue (PAAT), and decreased cortisol levels in the liver. HCD also causes the process of inflammatory fibrosis associated with the migration and spread of chromaffin cells in the adrenal gland. Conclusions This study gives new insights into how diet-induced obesity studied on local rabbits affects the biology of the adrenal gland. The correlation of these changes with paracrine connections between the chromaffin cell and glomerulosa indicates potential therapeutic methods for obese-related steroid hormone dysfunction.


2020 ◽  
Vol 98 (3) ◽  
pp. 177-181
Author(s):  
Yousef A. Bin Jardan ◽  
Ali Abdussalam ◽  
Ayman O.S. El-Kadi ◽  
Dion R. Brocks

Dronedarone biodistribution in hyperlipidemia and dronedarone metabolism in hyperlipidemia or obesity were assessed. Male Sprague–Dawley rats were given either normal standard chow with water or various high-fat or high-carbohydrate diets for 14 weeks. There was also a nonobese hyperlipidemic group given poloxamer 407 intraperitoneally. Liver and intestinal microsomes were prepared and the metabolic conversion of dronedarone to desbutyldronedarone was followed. A biodistribution study of dronedarone given orally was conducted in hyperlipidemic and control normolipidemic rats. The metabolism of dronedarone to desbutyldronedarone in control rats was consistent with substrate inhibition. However in the treatment groups, the formation of desbutyldronedarone did not follow substrate inhibition; hyperlipidemia and high-calorie diets created remarkable changes in dronedarone metabolic profiles and reduction in formation velocities. Tissue concentrations of dronedarone were much higher than in plasma. Furthermore, in hyperlipidemia, plasma and lung dronedarone concentrations were significantly higher compared to normolipidemia.


Author(s):  
O. Kalmukova ◽  
T. Kushmyruk ◽  
M. Dzerzhynsky

Kidneys, like the cardiovascular system, are one of the main target organs, the most vulnerable to obesity, because the first take on the metabolism correction function at an increasing excess of fat tissue in the body. Kidney affection under obesity is a multifactorial thing that is caused by a number of processes, including inflammation, oxidative stress, lipid metabolism disorders, renin-angiotensin-aldosterone system activation, insulin resistance and other factors. An optimal candidate for reducing the harmful effects of kidneys obesity should be a compound that simultaneously exhibits anti-inflammatory and antioxidant properties, controls the circadian rhythm, and also affects on the adipokines secretion. The molecule that meets these conditions is melatonin.The aim of our study was to determine morpho-functional state (morphology characteristic of kidney glomeruli and tubules; morphometric parameters: area and density of glomeruli) of kidney in rats with high-calorie (high fat) diet-induced obesity after melatonin administration in determined time of the day. Melatonin was administered daily by gavage for 7 weeks in dose 30 mg/kg 1 h before lights-off (ZT11) rats with high-calorie diet (HCD). Rats with HCD had huge changes in kidney morphology, which manifested in presence of numerous mesangial cells outside glomeruli and lipid droplets in tubules epithelial cells, while area and density of glomeruli in cm2 decrease. In general kidney with above mentioned characteristic from HCD rats lose their ability to conduct strongly renal function. After melatonin used in rats with HCD arise leveling of pathological changes, which associated with consumption of HCD. Namely, in rats with development obesity melatonin administrations led to increase area and density in comparison to HCD group, moreover glomeruli density reach control values. This is suggest that melatonin have protecting effect against glomerular degeneration. In conclusions, melatonin influence on kidney morpho-functional state in rats with HCD and turn back pathological its changes, moreover evening administration can use for obesity therapy via its strong action on conservation glomerular morphology.


2017 ◽  
Vol 8 (4) ◽  
pp. 377-390 ◽  
Author(s):  
Victoria V. Konopelniuk ◽  
Ievgenii I. Goloborodko ◽  
Tetyana V. Ishchuk ◽  
Tetyana B. Synelnyk ◽  
Ludmila I. Ostapchenko ◽  
...  

2008 ◽  
Vol 295 (2) ◽  
pp. R429-R435 ◽  
Author(s):  
Xiang Qi ◽  
Jason T. Reed ◽  
Guiyun Wang ◽  
Song Han ◽  
Ella W. Englander ◽  
...  

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.


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