scholarly journals Metformin ameliorates body mass gain and early metabolic changes in ovariectomized rats

2019 ◽  
Vol 8 (12) ◽  
pp. 1568-1578
Author(s):  
Clarissa Souza Barthem ◽  
Camila Lüdke Rossetti ◽  
Denise P Carvalho ◽  
Wagner Seixas da-Silva
Keyword(s):  
Insulin Resistance ◽  
Lipid Profile ◽  
Body Mass ◽  
Metabolic Diseases ◽  
Mass Gain ◽  
Ovariectomized Rats ◽  
Metabolic Dysfunction ◽  
Inactive Form ◽  
Female Wistar Rats ◽  
Risk Of Cancer

Estradiol has been used to prevent metabolic diseases, bone loss and menopausal symptoms, even though it might raise the risk of cancer. Metformin is usually prescribed for type 2 diabetes mellitus and lowers food intake and body mass while improving insulin resistance and the lipid profile. Ovariectomized rats show increased body mass, insulin resistance and changes in the lipid profile. Thus, the aim of this work was to evaluate whether metformin could prevent the early metabolic dysfunction that occurs early after ovariectomy. Female Wistar rats were divided into the following groups: SHAM-operated (SHAM), ovariectomized (OVX), ovariectomized + estradiol (OVX + E2) and ovariectomized + metformin (OVX + M). Treatment with metformin diminished approximately 50% of the mass gain observed in ovariectomized animals and reduced both the serum and hepatic triglyceride levels. The hepatic levels of phosphorylated AMP-activated protein kinase (pAMPK) decreased after OVX, and the expression of the inactive form of hepatic acetyl-CoA carboxylase (ACC) was also reduced. Metformin was able to increase the levels of pAMPK in the liver of OVX animals, sustaining the balance between the inactive and total forms of ACC. Estradiol effects were similar to those of metformin but with different proportions. Our results suggest that metformin ameliorates the early alterations of metabolic parameters and rescues hepatic AMPK phosphorylation and ACC inactivation observed in ovariectomized rats.

Ameliorative effect of low-dose spironolactone on obesity and insulin resistance is through replenishment of estrogen in ovariectomized rats

2019 ◽  
Vol 97 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Lawrence A. Olatunji ◽  
Oluwaseun A. Adeyanju ◽  
Olugbenga S. Michael ◽  
Taofeek O. Usman ◽  
Rita C. Tostes ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Low Dose ◽  
Glycogen Synthase ◽  
Mass Gain ◽  
Ovariectomized Rats ◽  
Atherogenic Dyslipidemia ◽  
Beneficial Effects ◽  
Ovx Rats ◽  
Ameliorative Effect ◽  
Hormonal Therapies

Women have a lower incidence of cardiovascular diseases (CVD) than men at a similar age but the reverse is the case after menopause, indicating a possible protective effect of estrogen on cardiometabolic function. Although various hormonal therapies have been formulated to combat the CVD risks in postmenopausal state, the beneficial effects have not been consistent. Obesity with insulin resistance (IR) is closely linked to CVD risks while ovariectomized rodents have been shown to mimic a state of obesity and IR. We therefore hypothesized that low-dose spironolactone would ameliorate obesity and IR in estrogen-deprived rats by replenishing estrogen and suppressing elevated glycogen synthase kinase-3 (GSK-3). Ten-week-old female Wistar rats were divided into 4 groups: sham-operated (SHM), spironolactone (SPL; 0.25 mg/kg), and ovariectomized (OVX) rats treated with or without spironolactone daily for 8 weeks. Results showed that estrogen deprivation through ovariectomy caused increased body mass gain and visceral adiposity that are accompanied by increased HOMA-IR, HOMA-β, 1-hour postload glucose, glucose intolerance, platelet/lymphocyte ratio, plasma insulin, atherogenic dyslipidemia, uric acid, GSK-3, corticosterone, and aldosterone and depressed 17β-estradiol. However, treatment of OVX rats with spironolactone ameliorated all these effects. Taken together, the results demonstrate that treatment with low-dose spironolactone improves obesity and IR, which appears to involve replenishment of estrogen and suppression of GSK-3 along with circulating mineralocorticoid and glucocorticoid. The findings imply a positive cardiometabolic effect of low-dose spironolactone usage in estrogen-deprived conditions.

scholarly journals The Interactive Effect of High Doses of Chromium(III) and Different Iron(III) Levels on the Carbohydrate Status, Lipid Profile, and Selected Biochemical Parameters in Female Wistar Rats

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3070
Author(s):  
Halina Zofia Staniek ◽  
Ewelina Król ◽  
Rafał Wojciech Wójciak
Keyword(s):  
Insulin Resistance ◽  
Lipid Profile ◽  
Carbohydrate Metabolism ◽  
Biochemical Parameters ◽  
Wistar Rats ◽  
Interactive Effect ◽  
The Other ◽  
Iron Deficient ◽  
Female Wistar Rats ◽  
High Doses

The aim of the study was to evaluate the main and interactive effects of chromium(III) propionate complex (Cr3) supplementation and different iron supply on the carbohydrate metabolism, lipid profile and other selected biochemical parameters of rats. The experiment was carried out in a two-factor design, in which rats were fed a diet with different proportions of Fe(III) and Cr(III) for six weeks. Fifty-four healthy female Wistar rats were divided into nine experimental groups with different Fe(III) levels, i.e. adequate—control group (45 mg/kg)—100% recommended daily dietary dose of Fe for rodents, deficient (5 mg/kg) and oversupply (180 mg/kg—400%). At the same time they were supplemented with Cr(III) of doses 1 (adequate), 50 and 500 mg/kg of diet. The activity and concentrations of most biochemical parameters were measured with standard enzymatic, kinetic, and colorimetric methods. HOMA-IR and QUICKI indexes were calculated according to appropriate formulas. It was found that there was an interactive effect of high Cr(III) doses and different Fe(III) levels in the diet on the carbohydrate metabolism and insulin resistance indexes. The presented results suggested that iron deficient diet fed animals led to insulin resistance; however, an effect is attenuated by Cr(III) supplementation at high doses. There were no significant changes in the rats’ lipid profile (except for the high density lipoprotein cholesterol (HDL-C) level) and most of the other biochemical parameters, such as the leptin, aspartate aminotransferase (AST), alanine transaminase (ALT), total protein (TP), creatinine (Crea) and the urea (BUN) concentrations. The study proved that the Cr(III) supplementation, independently and in combination with diversified Fe(III) content in the diet, affected the carbohydrate metabolism and insulin resistance indexes but did not affect lipid profile and most of the other biochemical parameters in healthy rats. The findings proved the role of Fe and Cr(III) and their interactions on disturbances carbohydrates metabolism.

scholarly journals The Role of the Immune System in Obesity and Insulin Resistance

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Payal S. Patel ◽  
Eric D. Buras ◽  
Ashok Balasubramanyam
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Immune System ◽  
Stress Responses ◽  
Innate Immune System ◽  
Metabolic Diseases ◽  
Innate Immune ◽  
Metabolic Dysfunction ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation

The innate immune system provides organisms with rapid and well-coordinated protection from foreign pathogens. However, under certain conditions of metabolic dysfunction, components of the innate immune system may be activated in the absence of external pathogens, leading to pathologic consequences. Indeed, there appears to be an intimate relationship between metabolic diseases and immune dysfunction; for example, macrophages are prime players in the initiation of a chronic inflammatory state in obesity which leads to insulin resistance. In response to increases in free fatty acid release from obese adipose depots, M1-polarized macrophages infiltrate adipose tissues. These M1 macrophages trigger inflammatory signaling and stress responses within cells that signal through JNK or IKKβpathways, leading to insulin resistance. If overnutrition persists, mechanisms that counteract inflammation (such as M2 macrophages and PPAR signaling) are suppressed, and the inflammation becomes chronic. Although macrophages are a principal constituent of obese adipose tissue inflammation, other components of the immune system such as lymphocytes and mast cells also contribute to the inflammatory cascade. Thus it is not merely an increased mass of adipose tissue that directly leads to attenuation of insulin action, but rather adipose tissue inflammation activated by the immune system in obese individuals that leads to insulin resistance.

scholarly journals Natural phenolic acids may increase serum estradiol level in ovariectomized rats.

2009 ◽  
Vol 56 (3) ◽  
Author(s):  
Maria Zych ◽  
Joanna Folwarczna ◽  
Henryk I Trzeciak
Keyword(s):  
Total Cholesterol ◽  
Body Mass ◽  
Phenolic Acids ◽  
Mass Gain ◽  
Estradiol Level ◽  
Ovariectomized Rats ◽  
Serum Estradiol ◽  
Chlorogenic Acids ◽  
Serum Estradiol Level ◽  
Cholesterol Levels

Natural phenolic acids are commonly present in plants consumed in the diet. Recently we have observed that different natural phenolic acids exert differential effects on the body mass gain in ovariectomized and non-ovariectomized female rats. The aim of the present study was to investigate the effects of ferulic, caffeic, p-coumaric and chlorogenic acids on serum estradiol and total cholesterol levels in ovariectomized and non-ovariectomized rats. The experiments were carried out on 3-month old female Wistar Cmd:(WI)WU rats, divided into following groups (n=8 in each group): non-ovariectomized control rats and non-ovariectomized rats receiving ferulic, caffeic, p-coumaric or chlorogenic acids, sham-operated control rats, ovariectomized control rats and ovariectomized rats receiving the same phenolic acids. The phenolic acids were administered at a dose of 10 mg/kg p.o. daily for 4 weeks. Serum estradiol and total cholesterol levels on the next day after the last administration of the phenolic acids were examined. The phenolic acids did not affect serum estradiol or total cholesterol levels in non-ovariectomized rats. In ovariectomized rats, caffeic acid and to a lesser extent p-coumaric acid increased serum estradiol level, which effect correlated with a decreased body mass gain. All the phenolic acids decreased serum cholesterol level in ovariectomized rats. Concluding, the anti-obesity activity of some phenolic acids may be, at least partially, connected with estrogenic pathways.

scholarly journals Effects of ERβ and ERα on OVX-induced changes in adiposity and insulin resistance

2020 ◽  
Vol 245 (1) ◽  
pp. 165-178 ◽  
Author(s):  
Terese M Zidon ◽  
Jaume Padilla ◽  
Kevin L Fritsche ◽  
Rebecca J Welly ◽  
Leighton T McCabe ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Estrogen Receptor ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Estrogen Receptor Alpha ◽  
Metabolic Diseases ◽  
Metabolic Effects ◽  
Metabolic Dysfunction ◽  
Gene And Protein Expression ◽  
Induced Changes

Loss of ovarian hormones leads to increased adiposity and insulin resistance (IR), increasing the risk for cardiovascular and metabolic diseases. The purpose of this study was to investigate whether the molecular mechanism behind the adverse systemic and adipose tissue-specific metabolic effects of ovariectomy requires loss of signaling through estrogen receptor alpha (ERα) or estrogen receptor β (ERβ). We examined ovariectomized (OVX) and ovary-intactwild-type (WT), ERα-null (αKO), and ERβ-null (βKO) female mice (age ~49 weeks; n = 7–12/group). All mice were fed a phytoestrogen-free diet (<15 mg/kg) and either remained ovary-intact (INT) or were OVX and followed for 12 weeks. Body composition, energy expenditure, glucose tolerance, and adipose tissue gene and protein expression were analyzed. INT αKO were ~25% fatter with reduced energy expenditure compared to age-matched INT WT controls and βKO mice (all P < 0.001). Following OVX, αKO mice did not increase adiposity or experience a further increase in IR, unlike WT and βKO, suggesting that loss of signaling through ERα mediates OVX-induced metabolic dysfunction. In fact, OVX in αKO mice (i.e., signaling through ERβ in the absence of ERα) resulted in reduced adiposity, adipocyte size, and IR (P < 0.05 for all). βKO mice responded adversely to OVX in terms of increased adiposity and development of IR. Together, these findings challenge the paradigm that ERα mediates metabolic protection over ERβ in all settings. These findings lead us to suggest that, following ovarian hormone loss, ERβ may mediate protective metabolic benefits.

Abstract 220: Exercise Training Attenuates Hypertension and Insulin Resistance in Old Fructose-fed Ovariectomized Rats

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Jacqueline F Machi ◽  
Nathalia Bernardes ◽  
Daniele S Dias ◽  
Ivana C Moraes-Silva ◽  
Fernando Dos Santos ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Adipose Tissue ◽  
Exercise Training ◽  
Wistar Rats ◽  
Physical Capacity ◽  
Ovariectomized Rats ◽  
Ovarian Hormone ◽  
Female Wistar Rats ◽  
Hormone Deprivation

Menopause and aging are associated with a gradual increase in systolic blood pressure. Poor eating habits through food containing fructose, have also been related to alterations in the cardiovascular system; however, there are few studies available in the literature relating exercise training (ET), menopause, aging and metabolic syndrome. The aim of the present study was to investigate the effects of ET in ovarian hormone deprivation and/or fructose consumption in old Wistar rats. Female Wistar rats (24 months old) were ovariectomized, fed with fructose (100g/L in drinking water) or normal water, and submitted to an ET protocol in treadmill (1 h/day; 5 days/wk for 8 wk, ~ 40-60% of maximum test) or kept sedentary. The groups were: ovariectomized (O, n= 8), ovariectomized trained (OT, n= 8), ovariectomized fructose (OF, n= 8) and ovariectomized fructose trained (OFT, n= 8). Glycemia, triglycerides, adipose tissue, insulin resistance, physical capacity and blood pressure (BP) were evaluated at the end of the protocol. While the glycemia values remained within the normal range (O:90.1±7.; OT:85.2±2; OF:86±2; OFT:80.6±3 mg/dl) and the triglycerides values were increased in OF group (OF:182±20 vs. O:140.3±9; OT:143.5±7;; OFT:140 ±12 mg/dl). The physical capacity was increased in both OFT (1.8±0.1 Km/h) and OF (1.6±0.07 Km/h) when compared with sedentary peers (O:1.1±0.05; OF: 1.1±0.05 Km/h). The metabolic results showed that ET decreased the adipose tissue in (OT: 6.7±0.9 and OFT: 5.28±0.6 vs. OF: 10.07±0.6 g), and insulin resistance (OT:4.8±0.2 and OFT: 5.0±0.2 vs. OF: 3.2±0.6 mg/dl/%). No differences were observed in O group (O: 6.5±0.8g and 4.5±0.2 mg/dl/min). Finally, ET attenuated the increase in mean BP in both OT and OFT rats (O:119±2; OT 110±2; OF:119±2; OFT: 107±1 mmHg). The same behavior was observed in systolic BP (O:142±2; OT 127±2; OF:143±2; OFT: 129±1 mmHg) and diastolic BP (O:100±2; OT 92±2; OF:98±2; OFT: 89±1 mmHg). In conclusion, low to moderate aerobic ET can attenuate the deleterious effects of ovarian hormone deprivation, and/or fructose consumption, especially the blood pressure increase in old female Wistar rats.

Beneficial effects of kinin B1 receptor antagonism on plasma fatty acid alterations and obesity in Zucker diabetic fatty rats

2016 ◽  
Vol 94 (7) ◽  
pp. 752-757 ◽  
Author(s):  
Sébastien Talbot ◽  
Jenny Pena Dias ◽  
Adil El Midaoui ◽  
Réjean Couture
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Body Mass ◽  
Mass Gain ◽  
Plasma Fatty Acid ◽  
B1 Receptor ◽  
Body Mass Gain ◽  
Zucker Diabetic Fatty Rats ◽  
Zdf Rats ◽  
The Impact

Kinins are the endogenous ligands of the constitutive B2 receptor (B2R) and the inducible B1 receptor (B1R). Whereas B2R prevents insulin resistance, B1R is involved in insulin resistance and metabolic syndrome. However, the contribution of B1R in type 2 diabetes associated with obesity remains uncertain. The aim of the present study was to examine the impact of 1-week treatment with a selective B1R antagonist (SSR240612, 10 mg/kg per day, by gavage) on hyperglycemia, hyperinsulinemia, leptinemia, body mass gain, and abnormal plasma fatty acids in obese Zucker diabetic fatty (ZDF) rats. Treatment with SSR240612 abolished the body mass gain and reduced polyphagia, polydipsia, and plasma fatty acid alterations in ZDF rats without affecting hyperglycemia, hyperinsulinemia, and hyperleptinemia. The present study suggests that the upregulated B1R plays a role in body mass gain and circulating fatty acid alterations in ZDF rats. However, mechanisms other than B1R induction would be implicated in glucose metabolism disorder in ZDF rats, based on the finding that SSR240612 did not reverse hyperglycemia and hyperinsulinemia.

Lipoic acid stimulates bone formation in ovariectomized rats in a dose-dependent manner

2016 ◽  
Vol 94 (9) ◽  
pp. 947-954 ◽  
Author(s):  
Radoslaw Piotr Radzki ◽  
Marek Bienko ◽  
Dariusz Wolski ◽  
Alicja Lis ◽  
Agnieszka Radzka
Keyword(s):  
Body Mass ◽  
Lipoic Acid ◽  
Experimental Treatment ◽  
Physiological Saline ◽  
Ovariectomized Rats ◽  
Sham Operation ◽  
Dependent Manner ◽  
Skeletal Density ◽  
Female Wistar Rats ◽  
Dose Dependent

This study was undertaken to determine the osteotropic effect of different doses of lipoic acid (LA) on the mineralization of bone tissue in female Wistar rats with experimental osteopenia induced by bilateral ovariectomy. Fifty-six rats were randomly selected and submitted to either a sham operation (n = 8) or an ovariectomy (n = 48). The ovariectomized rats were randomly placed into two control groups, treated subcutaneously with either physiological saline or 17β-estradiol in the dose of 4 μg/kg body mass per day, and four experimental groups that received LA subcutaneously in the doses of 12.5, 25, 50, and 100 mg/kg body mass per day (n = 8 in each group). After 28 days of experimental treatment, the rats were sacrificed, and body mass, total skeletal density, and body composition were recorded. Blood serum and isolated femora were stored for further analysis. Our results revealed that the osteoprotective effect of LA was dose-dependent and was observed in rats treated with 50 and 100 mg/kg of LA. Moreover, the LA applied to the ovariectomized rats in the dose of 50 mg/kg not only stopped the bone resorption, but stimulated its formation.

scholarly journals Prevention of Elevation in Plasma Triacylglycerol with High-Dose Bezafibrate Treatment Abolishes Insulin Resistance and Attenuates Glucose Intolerance Induced by Short-Term Treatment with Dexamethasone in Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-12
Author(s):  
Maiara Destro Inácio ◽  
Alex Rafacho ◽  
Nathália Aparecida de Paula Camaforte ◽  
Poliana Teixeira ◽  
Priscilla Maria Ponce Vareda ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Mass ◽  
Glucose Intolerance ◽  
Mass Gain ◽  
The Body ◽  
Lipid Lowering ◽  
High Dose ◽  
Short Term Treatment ◽  
Nonesterified Fatty Acids ◽  
Plasma Triacylglycerol

Objective. Fibrates are used as lipid-lowering drugs and are well tolerated as cotreatments when glucose metabolism disturbances are also present. Synthetic glucocorticoids (GCs) are diabetogenic drugs that cause dyslipidemia, dysglycemia, glucose intolerance, and insulin resistance when in excess. Thus, we aimed to describe the potential of bezafibrate in preventing or attenuating the adverse effects of GCs on glucose and lipid homeostasis. Methods. Male Wistar rats were treated with high-dose bezafibrate (300 mg/kg, body mass (b.m.)) daily for 28 consecutive days. In the last five days, the rats were also treated with dexamethasone (1 mg/kg, b.m.). Results. Dexamethasone treatment reduced the body mass gain and food intake, and bezafibrate treatment exerted no impact on these parameters. GC treatment caused an augmentation in fasting and fed glycemia, plasma triacylglycerol and nonesterified fatty acids, and insulinemia, and bezafibrate treatment completely prevented the elevation in plasma triacylglycerol and attenuated all other parameters. Insulin resistance and glucose intolerance induced by GC treatment were abolished and attenuated, respectively, by bezafibrate treatment. Conclusion. High-dose bezafibrate treatment prevents the increase in plasma triacylglycerol and the development of insulin resistance and attenuates glucose intolerance in rats caused by GC treatment, indicating the involvement of dyslipidemia in the GC-induced insulin resistance.

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