scholarly journals Genetic regulation of liver lipids in a mouse model of insulin resistance and hepatic steatosis

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Frode Norheim ◽  
Karthickeyan Chella Krishnan ◽  
Thomas Bjellaas ◽  
Laurent Vergnes ◽  
Calvin Pan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Mouse Model ◽  
Hepatic Steatosis ◽  
Genetic Regulation ◽  
Liver Lipids

scholarly journals Aberrant Hepatic Expression of PPARγ2 Stimulates Hepatic Lipogenesis in a Mouse Model of Obesity, Insulin Resistance, Dyslipidemia, and Hepatic Steatosis

2006 ◽  
Vol 281 (49) ◽  
pp. 37603-37615 ◽  
Author(s):  
Yuan-Li Zhang ◽  
Antonio Hernandez-Ono ◽  
Patty Siri ◽  
Stuart Weisberg ◽  
Donna Conlon ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Mouse Model ◽  
Hepatic Steatosis ◽  
Hepatic Lipogenesis ◽  
Hepatic Expression

scholarly journals Time-restricted feeding improves insulin resistance and hepatic steatosis in a mouse model of postmenopausal obesity

Metabolism ◽  
2016 ◽  
Vol 65 (12) ◽  
pp. 1743-1754 ◽  
Author(s):  
Heekyung Chung ◽  
Winjet Chou ◽  
Dorothy D. Sears ◽  
Ruth E. Patterson ◽  
Nicholas J.G. Webster ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Mouse Model ◽  
Hepatic Steatosis ◽  
Restricted Feeding ◽  
Postmenopausal Obesity

Effect of acetylsalicylic acid on inflamed adipose tissue. Insulin resistance and hepatic steatosis in a mouse model of diet-induced obesity

Life Sciences ◽  
2021 ◽  
Vol 264 ◽  
pp. 118618 ◽  
Author(s):  
Claudia Sardi ◽  
Elisa Martini ◽  
Tommaso Mello ◽  
Simone Camelliti ◽  
Lucia Sfondrini ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Mouse Model ◽  
Acetylsalicylic Acid ◽  
Hepatic Steatosis ◽  
Diet Induced Obesity

scholarly journals Metabolic PCOS Features Are Ameliorated by Mitochondrial Uncoupler BAM15 in a PCOS Mouse Model

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A769-A770
Author(s):  
Valentina Rodriguez Paris ◽  
Stephanie J Alexopoulos ◽  
Ying Hu ◽  
Divya P Shah ◽  
Ali Aflatounian ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Mouse Model ◽  
Hepatic Steatosis ◽  
Animal Studies ◽  
Metabolic Diseases ◽  
Polycystic Ovary ◽  
Mesenteric Fat ◽  
Adipocyte Hypertrophy ◽  
Mitochondrial Uncoupler

Abstract Polycystic ovary syndrome (PCOS) is a prevalent endocrine condition characterized by endocrine, reproductive and metabolic dysfunction. At present, there is no cure for PCOS and current treatments are suboptimal. Obesity and adverse metabolic features are prevalent in women with PCOS, with weight loss having a beneficial effect on PCOS features. The use of dietary interventions aimed at weight loss have low long-term compliance in women suffering from PCOS. Recent data from animal studies has shown that a small molecule mitochondrial uncoupler, BAM15, is an effective method to pharmacologically treat obesity and metabolic diseases. Therefore, the aim of this study was to investigate the efficacy of BAM15 to ameliorate PCOS-traits in a hyperandrogenic PCOS mouse model. As expected, exposure of female mice to dihydrotestosterone (DHT) induced the PCOS metabolic features of increased body weight (P<0.05), lean mass (P<0.001), increased parametrial and mesenteric fat pad weights (both P<0.05) and adipocyte hypertrophy (P<0.05). Additionally, DHT-induced PCOS mice exhibited insulin resistance measured by HOMA-IR, increased cholesterol and fasting triglyceride levels and hepatic steatosis (all P<0.05). In contrast, DHT-induced PCOS females treated with BAM15 displayed body weights which were comparable with controls, a significant decrease in parametrial and mesenteric fat depot weights (P<0.05) and reduced adipocyte hypertrophy. Furthermore, BAM15 treatment decreased insulin resistance, cholesterol and fasting triglyceride levels, as well as the degree of hepatic steatosis observed in PCOS females, to levels comparable with controls. PCOS mice presented the reproductive PCOS traits of irregular cycles and ovulatory dysfunction, however BAM15 did not improve these PCOS traits. These findings demonstrate that the pharmacologic mitochondrial uncoupler BAM15 is able to ameliorate metabolic PCOS features in a hyperandrogenic PCOS mouse model. These data provide compelling evidence to support BAM15 as a potential innovative and viable therapeutic approach to manage metabolic traits associated with PCOS.

scholarly journals Molecular Mechanisms of Hepatic Steatosis and Insulin Resistance in the AGPAT2-Deficient Mouse Model of Congenital Generalized Lipodystrophy

2009 ◽  
Vol 9 (2) ◽  
pp. 165-176 ◽  
Author(s):  
Víctor A. Cortés ◽  
David E. Curtis ◽  
Suja Sukumaran ◽  
Xinli Shao ◽  
Vinay Parameswara ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Mouse Model ◽  
Hepatic Steatosis ◽  
Molecular Mechanisms ◽  
Deficient Mouse ◽  
Congenital Generalized Lipodystrophy

1734-P: High Dietary Fat Intake Exacerbates Insulin Resistance in a Type 2 Diabetes Genetic Mouse Model

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1734-P
Author(s):  
AUSTIN REILLY ◽  
SHIJUN YAN ◽  
ALEXA J. LONCHARICH ◽  
HONGXIA REN
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Mouse Model ◽  
Dietary Fat ◽  
Fat Intake ◽  
Dietary Fat Intake ◽  
Genetic Mouse Model

scholarly journals INSIGHTS INTO THE ROLE OF MORUS ALBA IN REVERSING OBESITY-ASSOCIATED HEPATIC STEATOSIS AND RELATED METABOLIC DISORDER IN RATS

2016 ◽  
pp. 231
Author(s):  
Hanaa H. Ahmed ◽  
Fatehya M Metwally ◽  
Hend Rashad ◽  
Asmaa M Zaazaa
Keyword(s):  
Insulin Resistance ◽  
Hepatic Steatosis ◽  
Metabolic Disorder ◽  
Ethanolic Extract ◽  
Treated Group ◽  
Morus Alba ◽  
The Other ◽  
Obese Group ◽  
Control Group

<p>ABSTRACT<br />Objective: The goal of the present study was to examine the viability of Morus alba (M. alba) ethanolic extract in repression of obesity-associated<br />hepatic steatosis and related metabolic disorder; dyslipidemia, hyperinsulinemia, and glycemic status.<br />Methods: Adult female albino rats were randomly assigned into four groups, eight rats each as follows: Group (1) control group received standard<br />rodent diet for 24 weeks. The other three groups administered high cholesterol diet for 12 weeks and served as obese group, M. alba-treated group,<br />and simvastatin-treated group.<br />Results: The current results showed an increment in thoracic circumference (TCX) and abdominal circumferences (AC) as well as body mass index<br />(BMI) in obese group. In addition, dyslipidemia, hyperinsulinemia, hyperglycemia, and insulin resistance have been elucidated in obese group.<br />Moreover, hepatic malondialdehyde (MDA), nitric oxide (NO), serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and bilirubin<br />values were significantly increased in obese groups versus control group. On the other hand, administration of ethanolic extract of Morus alba or<br />simvastatin could significantly lessen BMI and in addition to improve dyslipidemia in obese group. Glucose, insulin levels, and insulin resistance value<br />in serum samples demonstrated a significant reduction in obese group upon treatment with M. alba ethanolic extract or simvastatin. Furthermore,<br />noticeable depletion in hepatic MDA, NO contents, serum ALT, AST activities, and serum bilirubin level was recorded as a result of treatment with<br />either ethanolic extract of M. alba or simvastatin. Histopathological examination of liver tissue showed ballooning degeneration in the hepatocytes<br />(hepatic steatosis) associated with inflammatory cells penetration in portal zone in obese group. Meanwhile, the treatment of obese groups with<br />ethanolic extract of M. alba or simvastatin was found to restore the structural organization of the liver.<br />Conclusion: The present findings provide a novel aspect for understanding of the role of M. alba against obesity-associated liver diseases and related<br />metabolic disorder. The mechanisms underlying these effects seem to depend on the hypolipidemic potential, anti-inflammatory property, and<br />antioxidant activity of its phytochemicals.<br />Keywords: Obesity, Morus alba, Dyslipidemia, Hyperinsulinemia, Hyperglycemia, Hepatic steatosis.</p>

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