Effect of Ursolic Acid on Insulin Resistance and Hyperinsulinemia in Rats with Diet-Induced Obesity: Role of Adipokines Expression

2020 ◽  
Vol 23 (3) ◽  
pp. 297-304 ◽  
Author(s):  
Angélica S. González-Garibay ◽  
Alfonso López-Vázquez ◽  
Jesús García-Bañuelos ◽  
Sergio Sánchez-Enríquez ◽  
Ana S. Sandoval-Rodríguez ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Ursolic Acid ◽  
Diet Induced Obesity

Sex-Specific Role of Adipose-Derived Lipocalin-2 in Diet-Induced Obesity and Insulin Resistance

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 285-LB ◽  
Author(s):  
KARTHICKEYAN CHELLA KRISHNAN ◽  
SIMON SABIR ◽  
RAQUEL FLOYD ◽  
DULSHAN JAYASEKERA ◽  
ALDONS LUSIS
Keyword(s):  
Insulin Resistance ◽  
Specific Role ◽  
Lipocalin 2 ◽  
Diet Induced Obesity

scholarly journals The Dualistic Effect of COX-2-Mediated Signaling in Obesity and Insulin Resistance

2019 ◽  
Vol 20 (13) ◽  
pp. 3115 ◽  
Author(s):  
Pei-Chi Chan ◽  
Min-Tser Liao ◽  
Po-Shiuan Hsieh
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
De Novo ◽  
Strongly Correlated ◽  
High Fat ◽  
Over Expression ◽  
Diet Induced Obesity ◽  
Key Enzyme ◽  
Cox 2

Obesity and insulin resistance are two major risk factors for the development of metabolic syndrome, type 2 diabetes and associated cardiovascular diseases (CVDs). Cyclooxygenase (COX), a rate-limiting enzyme responsible for the biosynthesis of prostaglandins (PGs), exists in two isoforms: COX-1, the constitutive form, and COX-2, mainly the inducible form. COX-2 is the key enzyme in eicosanoid metabolism that converts eicosanoids into a number of PGs, including PGD2, PGE2, PGF2α, and prostacyclin (PGI2), all of which exert diverse hormone-like effects via autocrine or paracrine mechanisms. The COX-2 gene and immunoreactive proteins have been documented to be highly expressed and elevated in adipose tissue (AT) under morbid obesity conditions. On the other hand, the environmental stress-induced expression and constitutive over-expression of COX-2 have been reported to play distinctive roles under different pathological and physiological conditions; i.e., over-expression of the COX-2 gene in white AT (WAT) has been shown to induce de novo brown AT (BAT) recruitment in WAT and then facilitate systemic energy expenditure to protect mice against high-fat diet-induced obesity. Hepatic COX-2 expression was found to protect against diet-induced steatosis, obesity, and insulin resistance. However, COX-2 activation in the epidydimal AT is strongly correlated with the development of AT inflammation, insulin resistance, and fatty liver in high-fat-diet-induced obese rats. This review will provide updated information regarding the role of COX-2-derived signals in the regulation of energy metabolism and the pathogenesis of obesity and MS.

scholarly journals Role of Muscle c-Jun NH2-Terminal Kinase 1 in Obesity-Induced Insulin Resistance

2009 ◽  
Vol 30 (1) ◽  
pp. 106-115 ◽  
Author(s):  
Guadalupe Sabio ◽  
Norman J. Kennedy ◽  
Julie Cavanagh-Kyros ◽  
Dae Young Jung ◽  
Hwi Jin Ko ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Wild Type ◽  
High Fat ◽  
Akt Activation ◽  
Peripheral Insulin Resistance ◽  
Diet Induced Obesity

ABSTRACT Obesity caused by feeding of a high-fat diet (HFD) is associated with an increased activation of c-Jun NH2-terminal kinase 1 (JNK1). Activated JNK1 is implicated in the mechanism of obesity-induced insulin resistance and the development of metabolic syndrome and type 2 diabetes. Significantly, Jnk1 − / − mice are protected against HFD-induced obesity and insulin resistance. Here we show that an ablation of the Jnk1 gene in skeletal muscle does not influence HFD-induced obesity. However, muscle-specific JNK1-deficient (MKO) mice exhibit improved insulin sensitivity compared with control wild-type (MWT) mice. Thus, insulin-stimulated AKT activation is suppressed in muscle, liver, and adipose tissue of HFD-fed MWT mice but is suppressed only in the liver and adipose tissue of MKO mice. These data demonstrate that JNK1 in muscle contributes to peripheral insulin resistance in response to diet-induced obesity.

The role of PPARγ in high-fat diet-induced obesity and insulin resistance

2002 ◽  
Vol 16 (1) ◽  
pp. 41-45 ◽  
Author(s):  
Takashi Kadowaki ◽  
Kazuo Hara ◽  
Naoto Kubota ◽  
Kazuyuki Tobe ◽  
Yasuo Terauchi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity

scholarly journals Exploring the role of ATP10A in diet‐induced obesity, insulin resistance, and type 2 diabetes

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Adriana Norris ◽  
Todd Graham ◽  
John Stafford ◽  
Lin Zhu
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Diet Induced Obesity

scholarly journals RGC32 deficiency protects against high-fat diet-induced obesity and insulin resistance in mice

2014 ◽  
Vol 224 (2) ◽  
pp. 127-137 ◽  
Author(s):  
Xiao-Bing Cui ◽  
Jun-Na Luan ◽  
Jianping Ye ◽  
Shi-You Chen
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Tolerance Test ◽  
High Fat ◽  
Diet Induced Obesity

Obesity is an important independent risk factor for type 2 diabetes, cardiovascular diseases and many other chronic diseases. Adipose tissue inflammation is a critical link between obesity and insulin resistance and type 2 diabetes and a contributor to disease susceptibility and progression. The objective of this study was to determine the role of response gene to complement 32 (RGC32) in the development of obesity and insulin resistance. WT and RGC32 knockout (Rgc32−/− (Rgcc)) mice were fed normal chow or high-fat diet (HFD) for 12 weeks. Metabolic, biochemical, and histologic analyses were performed. 3T3-L1 preadipocytes were used to study the role of RGC32 in adipocytes in vitro. Rgc32−/− mice fed with HFD exhibited a lean phenotype with reduced epididymal fat weight compared with WT controls. Blood biochemical analysis and insulin tolerance test showed that RGC32 deficiency improved HFD-induced dyslipidemia and insulin resistance. Although it had no effect on adipocyte differentiation, RGC32 deficiency ameliorated adipose tissue and systemic inflammation. Moreover, Rgc32−/− induced browning of adipose tissues and increased energy expenditure. Our data indicated that RGC32 plays an important role in diet-induced obesity and insulin resistance, and thus it may serve as a potential novel drug target for developing therapeutics to treat obesity and metabolic disorders.

scholarly journals Methotrexate attenuates vascular inflammation through an adenosine-microRNA dependent pathway

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Dafeng Yang ◽  
Stefan Haemmig ◽  
Haoyang Zhou ◽  
Daniel Pérez-Cremades ◽  
Xinghui Sun ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Vascular Endothelium ◽  
Vascular Inflammation ◽  
Vascular Diseases ◽  
High Dose ◽  
Dependent Manner ◽  
Diet Induced Obesity ◽  
Therapeutic Opportunity ◽  
Anti Inflammatory

Endothelial cell (EC) activation is an early hallmark in the pathogenesis of chronic vascular diseases. MicroRNA-181b (MiR-181b) is an important anti-inflammatory mediator in the vascular endothelium affecting endotoxemia, atherosclerosis, and insulin resistance. Herein, we identify that the drug methotrexate (MTX) and its downstream metabolite adenosine exert anti-inflammatory effects in the vascular endothelium by targeting and activating MiR-181b expression. Both systemic and endothelial-specific MiR-181a2b2-deficient mice develop vascular inflammation, white adipose tissue (WAT) inflammation, and insulin resistance in a diet-induced obesity model. Moreover, MTX attenuated diet-induced WAT inflammation, insulin resistance, and EC activation in a MiR-181a2b2-dependent manner. Mechanistically, MTX attenuated cytokine-induced EC activation through a unique adenosine-adenosine receptor A3-SMAD3/4-MiR-181b signaling cascade. These findings establish an essential role of endothelial MiR-181b in controlling vascular inflammation and that restoring MiR-181b in ECs by high dose MTX or adenosine signaling may provide a potential therapeutic opportunity for anti-inflammatory therapy.

scholarly journals Key Role of STAT4 Deficiency in the Hematopoietic Compartment in Insulin Resistance and Adipose Tissue Inflammation

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Anca D. Dobrian ◽  
Kaiwen Ma ◽  
Lindsey M. Glenn ◽  
Margaret A. Hatcher ◽  
Bronson A. Haynes ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Bone Marrow Cells ◽  
Cd8 Cells ◽  
Diet Induced Obesity ◽  
Hematopoietic Lineage ◽  
Islet Inflammation ◽  
Visceral Adipose

Visceral adipose tissue (AT) inflammation is linked to the complications of obesity, including insulin resistance (IR) and type 2 diabetes. Recent data from our lab showed that germline deficiency in STAT4 reduces inflammation and improves IR in obese mice. The objective of this study was to determine the contribution of selective STAT4 deficiency in subsets of hematopoietic cells to IR and AT inflammation. To determine the contribution of hematopoietic lineage, we sublethally irradiated Stat4−/−C57Bl6 mice and reconstituted them with bone marrow cells (BMC) from Stat4+/+C57Bl6 congenic donors. We also established the contribution of selective STAT4 deficiency in CD4+ or CD8+ T cells using adoptive transfer in Rag1−/− mice. All mice received a HFD for 15 weeks (n=7–12 mice/group). BMC that expressed STAT4 induced increases in glucose intolerance and IR compared to STAT4-deficient cells. Also, AT inflammation was increased and the numbers of CD8+ cells infiltrating AT were higher in mice with STAT4 expressing BMC. Studies in Rag1−/− mice further confirmed the prominent role of CD8+ cells expressing STAT4 in insulin resistance and AT and islet inflammation. Collectively our results show specific and dominant contribution of STAT4 in the hematopoietic compartment to metabolic health and inflammation in diet-induced obesity.

scholarly journals TRPM2 Ca2+ channel regulates energy balance and glucose metabolism

2012 ◽  
Vol 302 (7) ◽  
pp. E807-E816 ◽  
Author(s):  
Zhiyou Zhang ◽  
Wenyi Zhang ◽  
Dae Young Jung ◽  
Hwi Jin Ko ◽  
Yongjin Lee ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Gsk 3Β ◽  
Fat Feeding

TRPM2 Ca2+-permeable cation channel is widely expressed and activated by markers of cellular stress. Since inflammation and stress play a major role in insulin resistance, we examined the role of TRPM2 Ca2+ channel in glucose metabolism. A 2-h hyperinsulinemic euglycemic clamp was performed in TRPM2-deficient (KO) and wild-type mice to assess insulin sensitivity. To examine the effects of diet-induced obesity, mice were fed a high-fat diet for 4–10 mo, and metabolic cage and clamp studies were conducted in conscious mice. TRPM2-KO mice were more insulin sensitive partly because of increased glucose metabolism in peripheral organs. After 4 mo of high-fat feeding, TRPM2-KO mice were resistant to diet-induced obesity, and this was associated with increased energy expenditure and elevated expressions of PGC-1α, PGC-1β, PPARα, ERRα, TFAM, and MCAD in white adipose tissue. Hyperinsulinemic euglycemic clamps showed that TRPM2-KO mice were more insulin sensitive, with increased Akt and GSK-3β phosphorylation in heart. Obesity-mediated inflammation in adipose tissue and liver was attenuated in TRPM2-KO mice. Overall, TRPM2 deletion protected mice from developing diet-induced obesity and insulin resistance. Our findings identify a novel role of TRPM2 Ca2+ channel in the regulation of energy expenditure, inflammation, and insulin resistance.

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