scholarly journals Differentially Regulated Protein Kinase A (PKA) Activity in Adipose Tissue and Liver Is Associated With Resistance to Diet-Induced Obesity and Glucose Intolerance in Mice That Lack PKA Regulatory Subunit Type IIα

Endocrinology ◽  
2014 ◽  
Vol 155 (9) ◽  
pp. 3397-3408 ◽  
Author(s):  
Edra London ◽  
Maria Nesterova ◽  
Ninet Sinaii ◽  
Eva Szarek ◽  
Tatyana Chanturiya ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Protein Kinase ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
Regulatory Subunit ◽  
Wild Type ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Pka Regulatory Subunit ◽  
Kinase A

Abstract The cAMP-dependent protein kinase A (PKA) signaling system is widely expressed and has a central role in regulating cellular metabolism in all organ systems affected by obesity. PKA has four regulatory (RIα, RIIα, RIβ, RIIβ) and four catalytic (Cα, Cβ, Cγ, Prkx) subunit isoforms that have tissue-specific expression profiles. In mice, knockout (KO) of RIIβ, the primary PKA regulatory subunit in adipose tissue or knockout of the catalytic subunit Cβ resulted in a lean phenotype that resists diet-induced obesity and associated metabolic complications. Here we report that the disruption of the ubiquitously expressed PKA RIIα subunit in mice (RIIαKO) confers resistance to diet-induced obesity, glucose intolerance, and hepatic steatosis. After 2-week high-fat diet exposure, RIIαKO mice weighed less than wild-type littermates. Over time this effect was more pronounced in female mice that were also leaner than their wild-type counterparts, regardless of the diet. Decreased intake of a high-fat diet contributed to the attenuated weight gain in RIIαKO mice. Additionally, RIIα deficiency caused differential regulation of PKA in key metabolic organs: cAMP-stimulated PKA activity was decreased in liver and increased in gonadal adipose tissue. We conclude that RIIα represents a potential target for therapeutic interventions in obesity, glucose intolerance, and nonalcoholic fatty liver disease.

scholarly journals Deficiency of Growth Differentiation Factor 3 Protects against Diet-Induced Obesity by Selectively Acting on White Adipose

2009 ◽  
Vol 23 (1) ◽  
pp. 113-123 ◽  
Author(s):  
Joseph J. Shen ◽  
Lihua Huang ◽  
Liunan Li ◽  
Carolina Jorgez ◽  
Martin M. Matzuk ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Molecular Mechanisms ◽  
Normal Weight ◽  
Metabolic Rates ◽  
Wild Type ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Differentiation Factor ◽  
Tgfβ Superfamily

Growth differentiation factor 3 (GDF3) is a member of the TGFβ superfamily. White adipose is one of the tissues in which Gdf3 is expressed, and it is the only tissue in which expression increases in response to high-fat diet. We generated Gdf3−/− mice, which were indistinguishable from wild-type mice and had normal weight curves on regular diet. However, on high-fat diet Gdf3−/− mice were resistant to the obesity that normally develops in wild-type mice. Herein we investigate the physiological and molecular mechanisms that underlie this protection from diet-induced obesity and demonstrate that GDF3 deficiency selectively affects white adipose through its influence on basal metabolic rates. Our results are consistent with a role for GDF3 in adipose tissue, with consequential effects on energy expenditure that ultimately impact adiposity.

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.

Emodin Protects against High-Fat Diet-Induced Obesity via Regulation of AMP-Activated Protein Kinase Pathways in White Adipose Tissue

Planta Medica ◽  
2012 ◽  
Vol 78 (10) ◽  
pp. 943-950 ◽  
Author(s):  
Thing-Fong Tzeng ◽  
Hung-Jen Lu ◽  
Shorong-Shii Liou ◽  
Chia Chang ◽  
I-Min Liu
Keyword(s):  
Adipose Tissue ◽  
Protein Kinase ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Amp Activated Protein Kinase

scholarly journals Dietary Silk Peptide Prevents High-Fat Diet-Induced Obesity and Promotes Adipose Browning by Activating AMP-Activated Protein Kinase in Mice

Nutrients ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 201 ◽  
Author(s):  
Kippeum Lee ◽  
Heegu Jin ◽  
Sungwoo Chei ◽  
Jeong-Yong Lee ◽  
Hyun-Ji Oh ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Protein Kinase ◽  
High Fat Diet ◽  
Ex Vivo ◽  
Uncoupling Protein ◽  
Acid Oxidation ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Silk Peptide ◽  
Amp Activated Protein Kinase

Obesity is associated with metabolic syndrome and other chronic diseases, and is caused when the energy intake is greater than the energy expenditure. We aimed to determine the mechanism whereby acid-hydrolyzed silk peptide (SP) prevents high-fat diet-induced obesity, and whether it induces browning and fatty acid oxidation (FAO) in white adipose tissue (WAT), using in vivo and ex vivo approaches. We determined the effects of dietary SP in high-fat diet-fed obese mice. The expression of adipose tissue-specific genes was quantified by western blotting, qRT-PCR, and immunofluorescence analysis. We also investigated whether SP directly induces browning in primarily subcutaneous WAT-derived adipocytes. Our findings demonstrate that SP has a browning effect in WAT by upregulating AMP-activated Protein Kinase (AMPK) phosphorylation and uncoupling protein 1 (UCP1) expression. SP also suppresses adipogenesis and promotes FAO, implying that it may have potential as an anti-obesity drug.

Inhibitory Effects of Fermented Ougan (Citrus reticulata cv. Suavissima) Juice on High-Fat Diet-induced Obesity Associated with White Adipose Tissue Browning and Gut Microbiota Modulation in Mice

2021 ◽  
Author(s):  
Xiao Guo ◽  
Xuedan Cao ◽  
Xiugui Fang ◽  
Ailing Guo ◽  
Erhu Li
Keyword(s):  
Adipose Tissue ◽  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Citrus Reticulata ◽  
Inhibitory Effects ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Tissue Browning

In this study, Ougan juice (OJ) and lactic acid bacteria fermented Ougan juice (FOJ) were investigated individually for their capability of preventing obesity in high-fat diet (HFD)-fed C57BL/6J mice. After...

Trans-palmitoleic Acid Reduces Adiposity via Increased Lipolysis in a Rodent Model of Diet-Induced Obesity

2021 ◽  
pp. 1-24
Author(s):  
L. Irasema Chávaro-Ortiz ◽  
Brenda D. Tapia-Vargas ◽  
Mariel Rico-Hidalgo ◽  
Ruth Gutiérrez-Aguilar ◽  
María E. Frigolet
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Visceral Adipose Tissue ◽  
High Fat Diet ◽  
Palmitoleic Acid ◽  
Rodent Model ◽  
Adipocyte Size ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Visceral Adipose

Abstract Obesity is defined as increased adiposity, which leads to metabolic disease. The growth of adipose tissue depends on its capacity to expand, through hyperplasia or hypertrophy, in order to buffer energy surplus. Also, during the establishment of obesity, adipose tissue expansion reflects adipose lipid metabolism (lipogenesis and/or lipolysis). It is well known that dietary factors can modify lipid metabolism promoting or preventing the development of metabolic abnormalities that concur with obesity. Trans-palmitoleic acid (TP), a biomarker of dairy consumption, has been associated with reduced adiposity in clinical studies. Thus, we aimed to evaluate the effect of TP over adiposity and lipid metabolism-related genes in a rodent model of diet-induced obesity (DIO). To fulfil this aim, we fed C57BL/6 mice with a Control or a High Fat diet, added with or without TP (3g/kg diet), during 11 weeks. Body weight and food intake were monitored, fat pads were weighted, histology of visceral adipose tissue was analysed, and lipid metabolism-related gene expression was explored by qPCR. Results show that TP consumption prevented weight gain induced by high fat diet, reduced visceral adipose tissue weight, and adipocyte size, while increasing the expression of lipolytic molecules. In conclusion, we show for the first time that TP influences adipose tissue metabolism, specifically lipolysis, resulting in decreased adiposity and reduced adipocyte size in a DIO mice model.

scholarly journals Tissue-specific expression of Sprouty1 in mice protects against high-fat diet-induced fat accumulation, bone loss and metabolic dysfunction

2011 ◽  
Vol 108 (6) ◽  
pp. 1025-1033 ◽  
Author(s):  
Sumithra Urs ◽  
Terry Henderson ◽  
Phuong Le ◽  
Clifford J. Rosen ◽  
Lucy Liaw
Keyword(s):  
Adipose Tissue ◽  
Bone Loss ◽  
Bone Mass ◽  
Body Fat ◽  
High Fat Diet ◽  
Conditional Knockout ◽  
Whole Body ◽  
High Fat ◽  
Tissue Specific ◽  
Diet Induced Obesity

We recently characterised Sprouty1 (Spry1), a growth factor signalling inhibitor as a regulator of marrow progenitor cells promoting osteoblast differentiation at the expense of adipocytes. Adipose tissue-specific Spry1 expression in mice resulted in increased bone mass and reduced body fat, while conditional knockout of Spry1 had the opposite effect with decreased bone mass and increased body fat. Because Spry1 suppresses normal fat development, we tested the hypothesis that Spry1 expression prevents high-fat diet-induced obesity, bone loss and associated lipid abnormalities, and demonstrate that Spry1 has a long-term protective effect on mice fed a high-energy diet. We studied diet-induced obesity in mice with fatty acid binding promoter-driven expression or conditional knockout of Spry1 in adipocytes. Phenotyping was performed by whole-body dual-energy X-ray absorptiometry, microCT, histology and blood analysis. In conditional Spry1-null mice, a high-fat diet increased body fat by 40 %, impaired glucose regulation and led to liver steatosis. However, overexpression of Spry1 led to 35 % (P < 0·05) lower body fat, reduced bone loss and normal metabolic function compared with single transgenics. This protective phenotype was associated with decreased circulating insulin (70 %) and leptin (54 %; P < 0·005) compared with controls on a high-fat diet. Additionally, Spry1 expression decreased adipose tissue inflammation by 45 %. We show that conditional Spry1 expression in adipose tissue protects against high-fat diet-induced obesity and associated bone loss.

scholarly journals NT-PGC-1α Activation Attenuates High-Fat Diet–Induced Obesity by Enhancing Brown Fat Thermogenesis and Adipose Tissue Oxidative Metabolism

Diabetes ◽  
2014 ◽  
Vol 63 (11) ◽  
pp. 3615-3625 ◽  
Author(s):  
Hee-Jin Jun ◽  
Yagini Joshi ◽  
Yuvraj Patil ◽  
Robert C. Noland ◽  
Ji Suk Chang
Keyword(s):  
Adipose Tissue ◽  
Oxidative Metabolism ◽  
High Fat Diet ◽  
Brown Fat ◽  
High Fat ◽  
Diet Induced Obesity
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