Dyslipidemia’s influence on the secretion ovarian’s steroids in female mice

Introduction: The synthesis ovarian’s steroids is a process thats depends on the supply of cholesterol. Objective: to evaluate the influence of dyslipidemia on the secretion ovarian’s steroids. Methodology: wild female mice were used (C57BL6) and LDL (LDLR-/-), which they were separated into 4 groups (n = 10): WTS: fed a standard diet; WTHL: fed a high-fat diet; KOS: fed a standard diet; KOHL: fed a high-fat diet. After 60 days, the estrous cycle was analyzed and after anesthetized, blood was collected for the to assess the lipid profile, glucose, plasma insulin level and HOMA index was calculated. In addition, plasma levels of C-reactive protein, estrogen and progesterone were determined. Results: The hyperlipidic diet in both the WTHL and the KOHL group generated hypercholesterolemia when compared to the WTS and KOS, respectively, with a decrease in HDLc, associated with an increase in CRP levels. Severe hypercholesterolemia in the KOHL group generated insulin resistance, marked by an increase in HOMAir. Food hypercholesterolemia in the WTHL group, food and genetics in the KOHL group, compared to their WTS and KOS controls, was definitive in reducing plasma levels of estrogen and progesterone. The genetic hypercholesterolemia associated with insulin resistance observed in the KOS and KOHL groups reduced the levels of progesterone, this reduction being more severe in the KOHL group, which had the highest HOMAir. Conclusion: dyslipidemia affected ovarian steroidogenesis in mice by means of oxidative stress, inflammation and insulin resistance and / or by decreasing HDL cholesterol levels.

Download Full-text

Empagliflozin reverses obesity and insulin resistance through fat browning and alternative macrophage activation in mice fed a high-fat diet

BMJ Open Diabetes Research & Care ◽

10.1136/bmjdrc-2019-000783 ◽

2019 ◽

Vol 7 (1) ◽

pp. e000783 ◽

Cited By ~ 7

Author(s):

Liang Xu ◽

Naoto Nagata ◽

Guanliang Chen ◽

Mayumi Nagashimada ◽

Fen Zhuge ◽

...

Keyword(s):

Insulin Resistance ◽

Weight Gain ◽

Energy Expenditure ◽

Chronic Inflammation ◽

Plasma Levels ◽

High Fat Diet ◽

Macrophage Activation ◽

Low Grade ◽

Obese Mice ◽

High Fat

ObjectiveWe reported previously that empagliflozin—a sodium-glucose cotransporter (SGLT) 2 inhibitor—exhibited preventive effects against obesity. However, it was difficult to extrapolate these results to human subjects. Here, we performed a therapeutic study, which is more relevant to clinical situations in humans, to investigate antiobesity effects of empagliflozin and illustrate the mechanism underlying empagliflozin-mediated enhanced fat browning in obese mice.Research design and methodsAfter 8 weeks on a high-fat diet (HFD), C57BL/6J mice exhibited obesity, accompanied by insulin resistance and low-grade chronic inflammation. Cohorts of obese mice were continued on the HFD for an additional 8-week treatment period with or without empagliflozin.ResultsTreatment with empagliflozin for 8 weeks markedly increased glucose excretion in urine, and suppressed HFD-induced weight gain, insulin resistance and hepatic steatosis. Notably, empagliflozin enhanced oxygen consumption and carbon dioxide production, leading to increased energy expenditure. Consistently, the level of uncoupling protein 1 expression was increased in both brown and white (WAT) adipose tissues of empagliflozin-treated mice. Furthermore, empagliflozin decreased plasma levels of interleukin (IL)-6 and monocyte chemoattractant protein-1, but increased plasma levels of IL-33 and adiponectin in obese mice. Finally, we found that empagliflozin reduced M1-polarized macrophage accumulation, while inducing the anti-inflammatory M2 phenotype of macrophages in the WAT and liver, thereby attenuating obesity-related chronic inflammation.ConclusionsTreatment with empagliflozin attenuated weight gain by increasing energy expenditure and adipose tissue browning, and alleviated obesity-associated inflammation and insulin resistance by alternative macrophage activation in the WAT and liver of obese mice.

Download Full-text

Molecular factors involved in the hypolipidemic- and insulin-sensitizing effects of a ginger (Zingiber officinale Roscoe) extract in rats fed a high-fat diet

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2016-0374 ◽

2017 ◽

Vol 42 (2) ◽

pp. 209-215 ◽

Cited By ~ 21

Author(s):

Natalia de las Heras ◽

María Valero-Muñoz ◽

Beatriz Martín-Fernández ◽

Sandra Ballesteros ◽

Antonio López-Farré ◽

...

Keyword(s):

Lipid Profile ◽

Plasma Levels ◽

High Fat Diet ◽

Tissue Growth ◽

Collagen I ◽

Metabolic Effects ◽

Control Group ◽

Standard Diet ◽

High Fat ◽

Glucose Transporter 2

Hypolipidemic and hypoglycemic properties of ginger in animal models have been reported. However, information related to the mechanisms and factors involved in the metabolic effects of ginger at a hepatic level are limited. The aim of the present study was to investigate molecular factors involved in the hypoglycemic and hypolipidemic effects of a hydroethanolic ginger extract (GE) in the liver of rats fed a high-fat diet (HFD). The study was conducted in male Wistar rats divided into the following 3 groups: (i) Rats fed a standard diet (3.5% fat), the control group; (ii) rats fed an HFD (33.5% fat); and (iii) rats fed an HFD treated with GE (250 mg·kg−1·day−1) for 5 weeks (HFD+GE). Plasma levels of glucose, insulin, lipid profile, leptin, and adiponectin were measured. Liver expression of glycerol phosphate acyltransferase (GPAT), cholesterol 7 alpha-hydroxylase, peroxisome proliferator-activated receptors (PPAR), PPARα and PPARγ, glucose transporter 2 (GLUT-2), liver X receptor, sterol regulatory element-binding protein (SREBP1c), connective tissue growth factor (CTGF), and collagen I was measured. Data were analyzed using a 1-way ANOVA, followed by a Newman−Keuls test if differences were noted. The study showed that GE improved lipid profile and attenuated the increase of plasma levels of glucose, insulin, and leptin in HFD rats. This effect was associated with a higher liver expression of PPARα, PPARγ, and GLUT-2 and an enhancement of plasma adiponectin levels. Furthermore, GE reduced liver expression of GPAT, SREBP1c, CTGF, and collagen I. The results suggest that GE might be considered as an alternative therapeutic strategy in the management of overweight and hepatic and metabolic−related alterations.

Download Full-text

Palmitoleic Acid (N-7) Attenuates the Immunometabolic Disturbances Caused by a High-Fat Diet Independently of PPARα

Mediators of Inflammation ◽

10.1155/2014/582197 ◽

2014 ◽

Vol 2014 ◽

pp. 1-12 ◽

Cited By ~ 26

Author(s):

Camila O. Souza ◽

Alexandre A. S. Teixeira ◽

Edson A. Lima ◽

Helena A. P. Batatinha ◽

Lara M. Gomes ◽

...

Keyword(s):

Insulin Resistance ◽

Oleic Acid ◽

High Fat Diet ◽

Palmitoleic Acid ◽

Serum Levels ◽

Standard Diet ◽

Liver Inflammation ◽

Wild Type ◽

High Fat

Palmitoleic acid (PMA) has anti-inflammatory and antidiabetic activities. Here we tested whether these effects of PMA on glucose homeostasis and liver inflammation, in mice fed with high-fat diet (HFD), are PPAR-αdependent. C57BL6 wild-type (WT) and PPAR-α-knockout (KO) mice fed with a standard diet (SD) or HFD for 12 weeks were treated after the 10th week with oleic acid (OLA, 300 mg/kg of b.w.) or PMA 300 mg/kg of b.w. Steatosis induced by HFD was associated with liver inflammation only in the KO mice, as shown by the increased hepatic levels of IL1-beta, IL-12, and TNF-α; however, the HFD increased the expression of TLR4 and decreased the expression of IL1-Ra in both genotypes. Treatment with palmitoleate markedly attenuated the insulin resistance induced by the HFD, increased glucose uptake and incorporation into muscle in vitro, reduced the serum levels of AST in WT mice, decreased the hepatic levels of IL1-beta and IL-12 in KO mice, reduced the expression of TLR-4 and increased the expression of IL-1Ra in WT mice, and reduced the phosphorylation of NF𝜅B (p65) in the livers of KO mice. We conclude that palmitoleate attenuates diet-induced insulin resistance, liver inflammation, and damage through mechanisms that do not depend on PPAR-α.

Download Full-text

Swimming Exercise Alleviated Insulin Resistance by Regulating Tripartite Motif Family Protein 72 Expression and AKT Signal Pathway in Sprague-Dawley Rats Fed with High-Fat Diet

Journal of Diabetes Research ◽

10.1155/2016/1564386 ◽

2016 ◽

Vol 2016 ◽

pp. 1-9 ◽

Cited By ~ 7

Author(s):

Jie Qi ◽

Bo Yang ◽

Cailing Ren ◽

Jian Fu ◽

Jun Zhang

Keyword(s):

Insulin Resistance ◽

Protein Expression ◽

High Fat Diet ◽

Signal Pathway ◽

Swimming Exercise ◽

Standard Diet ◽

High Fat ◽

Expression Levels ◽

Family Protein ◽

Tripartite Motif

We aimed to investigate whether swimming exercise could improve insulin resistance (IR) by regulating tripartite motif family protein 72 (TRIM72) expression and AKT signal pathway in rats fed with high-fat diet. Five-week-old rats were classified into 3 groups: standard diet as control (CON), high-fat diet (HFD), and HFD plus swimming exercise (Ex-HFD). After 8 weeks, glucose infusion rate (GIR), markers of oxidative stress, mRNA and protein expression of TRIM72, protein of IRS, p-AKTSer473, and AKT were determined in quadriceps muscles. Compared with HFD, the GIR, muscle SOD, and GSH-Px were significantly increased (p<0.05, resp.), whereas muscle MDA and 8-OHdG levels were significantly decreased (p<0.05andp<0.01) in Ex-HFD. Expression levels of TRIM72 mRNA and protein in muscles were significantly reduced (p<0.05andp<0.01), whereas protein expression levels of IRS-1, p-AKTSer473, and AKT were significantly increased in Ex-HFD compared with HFD (p<0.01,p<0.01, andp<0.05). These results suggest that an 8-week swimming exercise improves HFD-induced insulin resistance maybe through a reduction of TRIM72 in skeletal muscle and enhancement of AKT signal transduction.

Download Full-text

Metabolic dysfunction in female mice with disruption of 5α-reductase 1

Journal of Endocrinology ◽

10.1530/joe-16-0125 ◽

2017 ◽

Vol 232 (1) ◽

pp. 29-36 ◽

Cited By ~ 10

Author(s):

Dawn E W Livingstone ◽

Emma M Di Rollo ◽

Tracy C-S Mak ◽

Karen Sooy ◽

Brian R Walker ◽

...

Keyword(s):

Insulin Resistance ◽

Hepatic Steatosis ◽

Stress Responses ◽

High Fat Diet ◽

Metabolic Dysfunction ◽

Male Mice ◽

High Fat ◽

Female Mice ◽

Normal Chow ◽

Transcript Profiles

5α-Reductases irreversibly catalyse A-ring reduction of pregnene steroids, including glucocorticoids and androgens. Genetic disruption of 5α-reductase 1 in male mice impairs glucocorticoid clearance and predisposes to glucose intolerance and hepatic steatosis upon metabolic challenge. However, it is unclear whether this is driven by changes in androgen and/or glucocorticoid action. Female mice with transgenic disruption of 5α-reductase 1 (5αR1-KO) were studied, representing a ‘low androgen’ state. Glucocorticoid clearance and stress responses were studied in mice aged 6 months. Metabolism was assessed in mice on normal chow (aged 6 and 12 m) and also in a separate cohort following 1-month high-fat diet (aged 3 m). Female 5αR1-KO mice had adrenal suppression (44% lower AUC corticosterone after stress), and upon corticosterone infusion, accumulated hepatic glucocorticoids (~27% increased corticosterone). Female 5αR1-KO mice aged 6 m fed normal chow demonstrated insulin resistance (~35% increased area under curve (AUC) for insulin upon glucose tolerance testing) and hepatic steatosis (~33% increased hepatic triglycerides) compared with controls. This progressed to obesity (~12% increased body weight) and sustained insulin resistance (~38% increased AUC insulin) by age 12 m. Hepatic transcript profiles supported impaired lipid β-oxidation and increased triglyceride storage. Female 5αR1-KO mice were also predisposed to develop high-fat diet-induced insulin resistance. Exaggerated predisposition to metabolic disorders in female mice, compared with that seen in male mice, after disruption of 5αR1 suggests phenotypic changes may be underpinned by altered metabolism of glucocorticoids rather than androgens.

Download Full-text

Lycopene Improves Insulin Sensitivity through Inhibition of STAT3/Srebp-1c-Mediated Lipid Accumulation and Inflammation in Mice fed a High-Fat Diet

Experimental and Clinical Endocrinology & Diabetes ◽

10.1055/s-0043-101919 ◽

2017 ◽

Vol 125 (09) ◽

pp. 610-617 ◽

Cited By ~ 22

Author(s):

Zhaohui Zeng ◽

Wang He ◽

Zhen Jia ◽

Shu Hao

Keyword(s):

Insulin Resistance ◽

Blood Glucose ◽

Lipid Accumulation ◽

High Fat Diet ◽

Fasting Blood Glucose ◽

Insulin Level ◽

Hepatic Glycogen ◽

High Fat ◽

Beneficial Effects ◽

Stat3 Signaling

AbstractIn the past few years, metabolic disorders, such as type 2 diabetes and metabolic syndrome, have reached global prevalence. Lycopene is one of the major carotenoids in tomatoes, watermelons, red grapefruits, and guava. In the current study, using high fat diet (HFD)-fed mice, we investigated the effect of Lycopene on insulin resistance. We showed that diet containing Lycopene significantly prevented HFD-induced increase of fasting blood glucose and insulin level, glucose and insulin intolerance, and decrease of hepatic glycogen content. We found that Lycopene notably prevented the increase of IL-1β, TNFα and CRP levels in mice fed HFD. We showed that Lycopene improved the lipid profiles in HFD-fed mice, as evidenced by decrease of systemic and hepatic TC, TG and LDL, and increase of HDL. Lycopene suppressed the increase of the expression of Srebp-1c, FAS and ACC-1 in mice fed HFD. The administration of Lycopene notably prevented the expression and phosphorylation of STAT3 in livers of mice induced by HFD. The treatment of adenovirus carrying STAT3 significantly suppressed the decrease of Srebp-1c expression induced by Lycopene. Furthermore, enhancement of STAT3 signaling by adenovirus markedly blocked the reduction of fasting blood glucose and insulin level. In conclusion, in the current study, we found that Lycopene prevented STAT3 signaling and inhibited Srebp-1c and downstream gene expression, resulting in inhibition of lipid accumulation, inflammation, insulin resistance and metabolic dysfunction. Overall, the data in the study provide better understanding of the beneficial effects of Lycopene against insulin resistance and metabolic disorder.

Download Full-text

Freeze-dried jaboticaba peel added to high-fat diet increases HDL-cholesterol and improves insulin resistance in obese rats

Food Research International ◽

10.1016/j.foodres.2012.07.052 ◽

2012 ◽

Vol 49 (1) ◽

pp. 153-160 ◽

Cited By ~ 55

Author(s):

Sabrina Alves Lenquiste ◽

Ângela Giovana Batista ◽

Rafaela da Silva Marineli ◽

Nathalia Romanelli Vicente Dragano ◽

Mário Roberto Maróstica

Keyword(s):

Insulin Resistance ◽

High Fat Diet ◽

Hdl Cholesterol ◽

High Fat ◽

Freeze Dried ◽

Obese Rats

Download Full-text

PENGARUH AROMATERAPI MINYAK ATSIRI JAHE TERHADAP KADAR TRIGLISERIDA DAN KOLESTEROL DARAH TIKUS YANG DIBERI PAKAN TINGGI LEMAK

Wahana Peternakan ◽

10.37090/jwputb.v1i2.41 ◽

2018 ◽

Vol 1 (2) ◽

Author(s):

Aji Agung Cahyaji

Keyword(s):

Essential Oil ◽

Total Cholesterol ◽

Cholesterol Level ◽

High Fat Diet ◽

Ldl Cholesterol ◽

Density Lipoprotein ◽

Hdl Cholesterol ◽

Albino Rats ◽

Standard Diet ◽

High Fat

The study aims to determine the effect of ginger (Zingiber officinale) essential oil via inhalation on blood triglyceride, total cholesterol, High Density Lipoprotein (HDL) cholesterol, and Low Density Lipoprotein (LDL) cholesterol level of rats that fed high fat diet. Eighteen albino rats (Rattus norvegicus) were devided into three treatments groups. The treatments were K1 (standard diet) as negative control, K2 (high fat diet) as positive control, and K3 (high fat diet + ginger essential oil inhalation). Blood samples were collected after 5 weeks of treatment period. The result showed the level of triglyceride, cholesterol, and HDL cholesterol at treatment K3 tend to be lower than treatment K2. LDL cholesterol level at treatment K3 show higher result than treatment K2. From the result of this study cocluded that inhalation of ginger essential oil can lowering triglyceride, total cholesterol, and LDL cholesterol level and raise HDL cholesterol level. Keywords: triglyceride, cholesterol, HDL cholesterol, LDL cholesterol, ginger essential oil

Download Full-text

Changes in Adiponectin and Inflammatory Genes in Response to Hormonal Imbalances in Female Mice and Exacerbation of Depot Selective Visceral Adiposity by High-Fat Diet: Implications for Insulin Resistance

Endocrinology ◽

10.1210/en.2007-0647 ◽

2007 ◽

Vol 148 (12) ◽

pp. 5667-5679 ◽

Cited By ~ 10

Author(s):

Hui Zhang ◽

Xinlei Chen ◽

Jayaprakash Aravindakshan ◽

M. Ram Sairam

Keyword(s):

Insulin Resistance ◽

Adipose Tissue ◽

Glucose Tolerance ◽

High Fat Diet ◽

Visceral Adiposity ◽

Protein Kinase Activity ◽

High Fat ◽

Inflammatory Genes ◽

Female Mice ◽

Mesenteric Fat

Early obesity and late onset of insulin resistance associated with hormonal imbalances occur in FSH receptor-deficient follitropin receptor knockout female mice. This study tests the hypothesis that chronic high-fat diet aggravates obesogenic changes in a depot-specific manner and explores some molecular links of hormone imbalances with insulin resistance. In SV 129 mice, hormonal imbalances seem obligatory for exacerbation of diet-induced obesity. Visceral adiposity, glucose intolerance, and lipid disturbances in 9-month follitropin receptor knockout females were associated with decrease in adiponectin signaling. High-molecular-weight plasma adiponectin and adipose tissue adiponectin mRNA were decreased. Adiponectin receptors R1 and R2 mRNA was selectively altered in mesenteric fat but not periuterine fat. R2 decreased in the liver and R1 was higher in muscle. Whereas hepatic adenosine monophosphate T-activated protein kinase activity was down-regulated, both phosphoenolpyruvate carboxykinase and glucose-6-phosphatase enzymes were up-regulated. Longitudinally, diminishing sex hormone signaling in adipose tissue was associated with progressive down-regulation of adiponectin activity and gradual impaired glucose tolerance. Chronic high-fat diet in SV129 wild-type mice did not produce overt obesity but induced visceral fat depot changes accompanied by liver lipid accumulation, high cholesterol, and up-regulation of inflammation gene mRNAs. Thus, TNF-α, C-C motif chemokine receptor-2, and C-C motif chemokine ligand-2 were selectively elevated in mesenteric fat without altering glucose tolerance and adiponectin signaling. Our study highlights adiponectin signaling and regulation to be involved in hormone imbalance-induced insulin resistance and demonstrates selective visceral adipose depot alterations by chronic high-fat diet and induction of inflammatory genes.

Download Full-text