Effects of cortisol and progesterone on insulin binding and lipogenesis in adipocytes from normal and diabetic rats

1985 ◽  
Vol 106 (2) ◽  
pp. 225-231 ◽  
Author(s):  
A.-M. Mendes ◽  
R. J. Madon ◽  
D. J. Flint
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Insulin Receptor ◽  
Body Weight Gain ◽  
Serum Insulin ◽  
Insulin Binding ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Receptor Concentration

ABSTRACT Cortisol implants in normal and diabetic rats reduced body weight, adiposity, insulin receptor concentration and both basal and insulin-stimulated rates of lipogenesis in isolated adipocytes, whilst insulin sensitivity was unchanged. In normal but not diabetic rats these changes were accompanied by increased serum glucose and insulin concentrations. In contrast, progesterone implants in normal and diabetic rats increased body weight gain, adiposity, insulin receptor concentration and both basal and insulin-stimulated rates of lipogenesis in adipose tissue, again without affecting insulin sensitivity. Progesterone did not affect serum insulin concentrations in normal or diabetic rats but accelerated the decline in serum glucose concentrations which occurred during an overnight fast in diabetic rats. The results suggest that (1) cortisol inhibits lipogenesis in adipose tissue without affecting insulin sensitivity, (2) cortisol reduces insulin binding in adipose tissue without a requirement for hyperinsulinaemia, which might itself indirectly lead to down-regulation of the insulin receptor, and (3) in diabetic rats progesterone stimulates lipogenesis in adipose tissue without any increase in food intake or serum insulin concentrations suggesting that progesterone may have a direct anabolic role in adipose tissue. J. Endocr. (1985) 106, 225–231

scholarly journals Adipose tissue transplantation protects ob/ob mice from obesity, normalizes insulin sensitivity and restores fertility

2005 ◽  
Vol 186 (1) ◽  
pp. 203-211 ◽  
Author(s):  
Simon Klebanov ◽  
Clinton M Astle ◽  
Olga DeSimone ◽  
Vitaly Ablamunits ◽  
David E Harrison
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Therapeutic Potential ◽  
Body Weight Gain ◽  
Hormone Replacement ◽  
Tolerance Test ◽  
Reduced Body ◽  
Insulin Tolerance

Adipose tissue affects metabolism by secreting various adipokines. Lipodystropic mice benefit both from leptin replacement therapy and from transplantation of normal fat. Leptin-deficient Lepob/Lepob (ob/ob) mice can also be treated with leptin. Surprisingly, there have been no reports of successful treatment of obese ob/ob mice by transplantation of normal white adipose tissue (WAT). If WAT transplantation is ineffective in treating insulin resistance and diabetes in obese individuals, its applicability may be limited in humans as such abnormalities are usually associated with obesity. In the current study, we tested whether WAT transplantation might prevent, and even reverse, abnormalities characteristic of ob/ob mice. To assess the preventive potential, 6-week-old ob/ob mice were transplanted, subcutaneously, with gonadal fat pads from normal mice. Profound effects on multiple physiological phenotypes were achieved despite leptin levels below 25% of those in control mice. WAT from one donor reduced body weight gain, and WAT from 4 or 8 donors prevented obesity in ob/ob mice. Nonfasting insulin levels and insulin tolerance test were normalized. Corticosterone elevation was also prevented. Finally, WAT from 4 donors restored fertility in ob/ob females. The effects of WAT transplantation were long-lasting, with body weight gain suppressed for at least 40 weeks. To assess the therapeutic potential, obese 13-month-old ob/ob mice with a long history of leptin deficiency were used. Their body weight decreased by approximately 50% when transplanted with WAT from 8 donors. As in young recipients, transplantation greatly reduced nonfasting insulin, suggesting normalized insulin sensitivity. Thus, WAT transplantation was effective for both prevention and therapy. In the future, WAT transplantation may become a useful alternative to hormone replacement in treating not only lipodystropy, but also certain types of obesity.

Rosa rugosa Attenuates Diabetic Oxidative Stress in Rats with Streptozotocin-Induced Diabetes

2004 ◽  
Vol 32 (04) ◽  
pp. 487-496 ◽  
Author(s):  
Eun Ju Cho ◽  
Takako Yokozawa ◽  
Hyun Young Kim ◽  
Naotoshi Shibahara ◽  
Jong Cheol Park
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Body Weight Gain ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Radical Scavenger ◽  
Thiobarbituric Acid Reactive Substance ◽  
Rosa Rugosa

The effects of Rosa rugosa on diabetic oxidative stress were investigated using rats with streptozotocin (STZ)-induced diabetes. The diabetic rats showed less body weight gain and heavier kidney and liver weights than normal rats, while the oral administration of Rosa rugosa at a dose of 100 or 200 mg/kg body weight/day for 20 days attenuated the physiological changes induced by diabetes. In addition, administrating Rosa rugosa to diabetic rats resulted in significant and dose-dependent decreases in the serum glucose and glycosylated protein levels, implying that Rosa rugosa improves the abnormal glucose metabolism that leads to oxidative stress. Diabetic rats had higher serum levels of superoxide and nitrite/nitrate. However, the administration of Rosa rugosa dose-dependently reduced the over-production of radicals associated with diabetes, suggesting Rosa rugosa is a radical scavenger that would play a crucial role in protecting against diabetic oxidative stress. Rosa rugosa significantly and dose-dependently reduced thiobarbituric acid-reactive substance levels in serum, hepatic and renal mitochondria, implying that Rosa rugosa would alleviate the oxidative stress associated with diabetes by inhibiting lipid peroxidation. This study provides evidence that Rosa rugosa has potential as a treatment for diabetes through attenuating oxidative stress induced by the diabetic condition

Increased sensitivity of the genetically obese mouse to corticosterone

1987 ◽  
Vol 252 (2) ◽  
pp. E202-E208 ◽  
Author(s):  
K. Tokuyama ◽  
J. Himms-Hagen
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Body Weight Gain ◽  
Serum Insulin ◽  
Obese Mouse ◽  
Serum Corticosterone ◽  
Brown Adipose

Adrenalectomy normalizes many abnormalities of the obese (ob/ob) mouse. The high corticosterone concentration in blood may account in part for development of obesity and other abnormalities in the ob/ob mouse. Our objective was to determine dose-response relationships for the effect of corticosterone on the obesity. Lean and ob/ob mice were adrenalectomized or sham-operated at 4.5 wk of age. Adrenalectomized mice received 100 mg implants of cholesterol containing corticosterone (0, 2, 5, 20, or 50 mg) at 8.5 wk of age and were killed at 10.5 wk of age. In ob/ob mice, but not in lean mice, low physiological levels of serum corticosterone (up to 10 micrograms/dl) markedly increased body weight gain, food intake, and serum insulin. They also increased white and brown adipose tissue weights and decreased brown adipose tissue mitochondrial GDP binding. Higher levels of corticosterone (12-22 micrograms/dl) increased body weight gain, white and brown adipose tissue weights, and serum insulin and suppressed brown adipose tissue mitochondrial GDP binding in lean mice also, although in most cases to a lesser extent than in ob/ob mice, but were still without effect on food intake. Only very high levels of corticosterone (approximately 30 micrograms/dl) increased food intake in lean mice. Hyperglycemia was induced in ob/ob, but not lean, mice only at concentrations of corticosterone greater than 17 micrograms/dl. Thermoregulation was unaffected by serum corticosterone at levels from 0 to 30 micrograms/dl in both ob/ob and lean mice. Thus the ob/ob mouse is excessively sensitive and responsive to an effect of physiological levels of corticosterone that results in hyperphagia, hyperinsulinemia, and increased weight gain.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of body weight gain on insulin sensitivity after retirement from exercise training

1990 ◽  
Vol 68 (2) ◽  
pp. 520-526 ◽  
Author(s):  
C. B. Dolkas ◽  
K. J. Rodnick ◽  
C. E. Mondon
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Body Weight Gain ◽  
Liver Glycogen ◽  
Serum Glucose ◽  
Hypocaloric Diet ◽  
Oral Glucose ◽  
Steady State Serum

The objectives of this study were to determine how long increased insulin sensitivity, elicited by exercise training, persists after the end of training and what the effect of weight gain is on this retention. Exercise-trained (ET) rats ran voluntarily in freely rotating wheel cages, and insulin sensitivity was assessed by oral glucose tolerance tests (OGTT) and insulin suppression tests (IST). After training, ET rats were retired for 1, 3, or 7 days (R1, R3, or R7). Initial OGTT and IST studies indicated that sensitivity to insulin-induced glucose uptake was increased in ET rats compared with sedentary control (C) rats and was progressively lost with retirement: ET greater than R1 and R3 greater than R7 and C rats, and this reaction was generally associated with a rapid gain in body weight. Subsequent IST tests were performed on C and R7 rats fed laboratory chow or a hypocaloric diet consisting of equal parts of cellulose and chow for 7 days before the test. The results of these tests showed that steady-state serum glucose (SSSG) levels averaged 165 +/- 12 mg/dl for chow-fed C rats and 172 +/- 11 mg/dl for chow-fed R7 rats that gained body weight at rates twice those of C rats. Chow-fed R7 rats, gaining weight at rates comparable to C rats, had SSSG levels of 104 +/- 6 mg/dl. C and R7 rats fed the hypocaloric diet had SSSG values of 102 +/- 6 and 59 +/- 4 mg/dl, respectively. Muscle glycogen levels were comparable in all groups, and liver glycogen was lower in C and R7 rats fed the hypocaloric diet.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Loss of voltage-gated proton channel Hv1 leads to diet-induced obesity in mice

2020 ◽  
Vol 8 (1) ◽  
pp. e000951
Author(s):  
Huimin Pang ◽  
Jinwen Li ◽  
Hongyan Du ◽  
Yingtang Gao ◽  
Jili Lv ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Body Weight Gain ◽  
Proton Channel ◽  
Gene Expressions ◽  
Voltage Gated ◽  
Diet Induced Obesity ◽  
Obesity In Mice ◽  
Genetic Deletion

ObjectiveThe voltage-gated proton channel Hv1 has been proposed to mediate NADPH oxidase (NOX) function by regulating intracellular pH during respiratory bursts. In our previous work, we showed that Hv1 is expressed in pancreatic β cells and positively regulates insulin secretion. Here, we investigated the role of Hv1 in adipose tissue differentiation, metabolic homeostasis and insulin sensitivity using Hv1 knockout (KO) mice.DesignMice with genetic deletion of Hv1 are treated with high-fat diet (HFD) similar to wild-type (WT) mice. Body weight gain, adiposity, insulin sensitivity and gene expressions in both adipose tissue and liver were analyzed.ResultsMice with genetic deletion of Hv1 display overt obesity with higher body weight gain and accumulation of adipose tissue compared with similarly HFD-treated WT. Hv1-deficient mice develop more glucose intolerance than WT, but no significant difference in insulin resistance, after fed with HFD. Deficiency of Hv1 results in a remarkable increase in epididymal adipocyte weight and size, while the gene expressions of proinflammatory factors and cytokines are obviously enhanced in the HFD-fed mice. Furthermore, the gene expression of Hv1 is increased in the HFD-fed mice, which is accompanied by the increase of NOX2 and NOX4. In addition, there is more severely diet-induced steatosis and inflammation in liver in KO mice.ConclusionOur data demonstrated that lacking of Hv1 results in diet-induced obesity in mice through inflammation and hepatic steatosis. This study suggested that Hv1 acts as a positive regulator of metabolic homeostasis and a potential target for antiobesity drugs in therapy and may serve as an adaptive mechanism in cooperating with NOX to mediate reactive oxygen species for adipogenesis and insulin sensitivity.

scholarly journals SAT-586 Cold-Acclimation Prevents the Onset of Glucocorticoid-Induced Adipose Dysfunction in Male Mice

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Manuel M Gado ◽  
Monique Noll ◽  
Annett Heinrich ◽  
Martina Rauner ◽  
Lorenz C Hofbauer ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Cold Acclimation ◽  
Environmental Temperature ◽  
Body Weight Gain ◽  
Serum Insulin ◽  
Metabolic Dysfunction ◽  
Temperature Levels ◽  
Thermogenic Capacity

Abstract Glucocorticoid (GC) excess, either endogenously or exogenously, has been causally linked to the development of chronic diseases such as obesity and type-2 diabetes mellitus. Continuously elevated GC levels result in an expansion of white adipose tissue (WAT) depots and a dramatic decrease in the thermogenic capacity in brown and beige adipose tissue (BAT and BeAT, respectively). Herein we aimed to examine the interaction between GCs and the sympathetic nervous system (SNS) in the regulation of WAT, BAT, and BeAT. To this end, we utilized an altered environmental temperature as a non-invasive method for the modulation of sympathetic activity - cold is an activator of SNS-mediated non-shivering thermogenesis. Thus, during a 4-week treatment with either corticosterone or placebo, 10-week-old male C57BL/6NRj mice were maintained at two different temperature levels: 29°C (thermoneutrality) or 13°C (cold temperature). Body weight, as well as energy and water intake, were monitored throughout the study. At sacrifice, serum and adipose tissues were collected for analysis. GC-exposed mice showed a marked increase in circulating corticosterone concentrations compared to placebo controls with no appreciable difference between temperature levels. At thermoneutrality, GC-treated mice gained more weight and consumed more food than their placebo-treated littermates. This GC-induced body weight gain was accompanied by increased (visceral & subcutaneous) WAT weight as well as adipocyte hypertrophy. Interestingly, cold-acclimatized mice showed a marked reduction in GC-induced weight gain, hyperphagia, and fat accumulation. Moreover, the GC-induced rise in blood glucose and serum insulin concentrations - readily observed when mice were maintained at thermoneutrality - was absent in cold-exposed animals. In addition, GC treatment at thermoneutrality resulted in increased lipid deposition and decreased UCP1 expression in BAT, the ‘whitening’ of BAT. This GC-induced loss of thermogenic capacity was profoundly reduced in cold-adapted mice. Across all groups, UCP-1 protein levels in BAT closely correlated (r2 = 0.70, p < 0.0001) with those of tyrosine hydroxylase (TH), the rate-limiting enzyme of catecholamine synthesis. These results indicate that cold-acclimation prevents the development of GC-induced metabolic dysfunction in mice. Thus, environmental temperature is a potent modulator of GC-induced adiposity and body weight gain, potentially via an interaction between SNS and GC signaling.

Hepato-renal protective effects of gallic acid and p-coumaric acid in nicotinamide/streptozotocin-induced diabetic rats

2016 ◽  
Vol 5 (06) ◽  
pp. 4641 ◽  
Author(s):  
Adel Abdel Moneim* ◽  
Sanaa M. Abd El-Twab ◽  
Mohamed B. Ashour ◽  
Ahmed I. Yousef
Keyword(s):  
Body Weight ◽  
Gallic Acid ◽  
Protein Profile ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Hypoglycemic Agents ◽  
Protective Effects ◽  
Coumaric Acid ◽  
Experimental Type

The goal of diabetes treatment is primarily to save life and alleviate symptoms and secondary to prevent long-term diabetic complications resulting from hyperglycemia. Thus, our present investigation was designed to evaluate the hepato-renal protective effects of gallic acid and p-coumaric acid in nicotinamide/streptozotocin (NA/STZ)-induced diabetic rats. Experimental type 2 diabetes was induced by a single intraperitoneal (i.p.) injection of STZ (65 mg/kg b.wt.), after 15 min of i.p. injection of NA (120 mg/kg b.wt.). Gallic acid and p-coumaric acid were orally administered to diabetic rats at a dose of 20, 40 mg/kg b.wt./day, respectively, for 6 weeks. Body weight, serum glucose, protein profile, liver function enzymes and kidney function indicators was assayed. Treatment with either gallic acid or p-coumaric acid significantly ameliorated the elevated levels of glucose, alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea and uric acid. Both compounds were also found to restore total protein, albumin, and globulin as well as body weight of diabetic rats to near normal values. It can conclude that both gallic acid and p-coumaric acid have potent hypoglycemic and hepato-renal protective effects in diabetic rats. Therefore, our results suggest promising hypoglycemic agents that can attenuate the progression of diabetic hepatopathy and nephropathy.

scholarly journals Interleukin-6 mediated exercise-induced alleviation of adiposity and hepatic steatosis in mice

2021 ◽  
Vol 9 (1) ◽  
pp. e001431
Author(s):  
Long Li ◽  
Caoxin Huang ◽  
Hongyan Yin ◽  
Xiaofang Zhang ◽  
Dongmei Wang ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Exercise Training ◽  
Hepatic Steatosis ◽  
Interleukin 6 ◽  
Body Weight Gain ◽  
Treadmill Running ◽  
Alcoholic Fatty Liver ◽  
Fat Accumulation ◽  
Ppar Γ

IntroductionExercise training has been shown to be the most effective strategy to combat obesity and non-alcoholic fatty liver disease. However, exercise promotes loss of adipose tissue mass and improves obesity-related hepatic steatosis through mechanisms that remain obscure.Research design and methodsTo study the role of interleukin-6 (IL-6) in high-fat diet (HFD)-induced adiposity and hepatic steatosis during treadmill running, IL-6 knockout (IL-6 KO) mice and wild-type (WT) mice were randomly divided into lean, obese (fed a HFD) and trained obese groups (fed a HFD and exercise trained).ResultsAfter 20 weeks of HFD feeding and 8 weeks of treadmill running, we found that exercise obviously reduced HFD-induced body weight gain, inhibited visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) expansion and almost completely reversed obesity-related intrahepatic fat accumulation in WT mice. However, IL-6 knockout (IL-6 KO) mice are refractory to the benefits of treadmill training on body weight, VAT and SAT mass elevation, and hepatic steatosis. Moreover, a panel of lipolytic-related and thermogenic-related genes, including ATGL, HSL and PGC-1α, was upregulated in the VAT and SAT of WT mice that received exercise training compared with untrained mice, which was not observed in IL-6 KO mice. In addition, exercise training resulted in a significant inhibition of hepatic peroxisome proliferator-activated receptor gamma (PPAR-γ) expression in WT mice, and these effects were not noted in IL-6 KO mice.ConclusionThese results revealed that IL-6 is involved in the prevention of obesity and hepatic fat accumulation during exercise training. The mechanisms underlying these antiobesity effects may be associated with enhanced lipolysis and thermogenesis in white adipose tissue. The improvement in hepatic steatosis by exercise training may benefit from the marked inhibition of PPAR-γ expression by IL-6.

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