scholarly journals Ketone esters increase brown fat in mice and overcome insulin resistance in other tissues in the rat

2013 ◽  
Vol 1302 (1) ◽  
pp. 42-48 ◽  
Author(s):  
Richard L. Veech
Keyword(s):  
Insulin Resistance ◽  
Brown Fat

The development of insulin resistance in brown adipose tissue may impair the acute cold-induced activation of thermogenesis in genetically obese (ob/ob) mice

1984 ◽  
Vol 4 (11) ◽  
pp. 933-940 ◽  
Author(s):  
Stewart W. Mercer ◽  
Paul Trayhurn
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Brown Fat ◽  
Acute Cold Exposure ◽  
Brown Adipose

Genetically obese (ob/ob) mice develop insulin resistance in brown adipose tissue during the fifth week of life. Prior to this, at 26 days of age, oh/oh mice show a substantial increase in GDP binding to brownadipose-tissue mitochondria during acute cold exposure. When insulin resistance in brown fat develops, by 35 days of age, the increase in GDP binding in response to cold is markedly reduced. Studies with 2-deoxyglucose suggest that insulin resistance in brown adipose tissue could impair thermogenic responsiveness during acute cold exposure by limiting the ability of the tissue to take up glucose.

Changes in adipokine expression during food deprivation in the mouse and the relationship to fasting-induced insulin resistance

2003 ◽  
Vol 81 (10) ◽  
pp. 979-985 ◽  
Author(s):  
Yaoting Gui ◽  
Josef V Silha ◽  
Suresh Mishra ◽  
Liam J Murphy
Keyword(s):  
Insulin Resistance ◽  
Food Deprivation ◽  
Tissue Expression ◽  
Brown Fat ◽  
Mrna Abundance ◽  
Peroxisome Proliferator ◽  
Mrna Levels ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ ◽  
Plasma Leptin

We investigated the changes in insulin resistance and adipose tissue expression of the adipokines resistin, adiponectin, and leptin and the transcription factors peroxisome proliferator-activated receptor-γ (PPAR-γ) and retinoid X receptor-α (RXR-α) during 48 h of food deprivation. Insulin sensitivity (SI) declined, whereas glucose effectiveness (SG) increased. Plasma adiponectin levels declined in the first 8 h and remained constant thereafter. There was no correlation between either SI or SG and adiponectin protein or mRNA levels. PPAR-γ mRNA abundance remained constant, whereas leptin and resistin mRNAs and plasma leptin declined and RXR-α mRNA abundance increased in both white and brown fat. Leptin mRNA abundance was closely correlated with SI (R2 = 0.91 and 0.87 for white and brown fat, respectively). Resistin mRNA abundance correlated inversely with SG (R2 = 0.99 and 0.84 for white and brown fat, respectively). These data indicate that changes in the expression of leptin are more closely correlated with the insulin resistance of fasting than with changes in other adipokines or RXR-α and PPAR-γ expression.Key words: insulin resistance, fasting, adipokines, resistin, leptin, adiponectin.

scholarly journals Brown Fat Lipoatrophy and Increased Visceral Adiposity through a Concerted Adipocytokines Overexpression Induces Vascular Insulin Resistance and Dysfunction

Endocrinology ◽  
2012 ◽  
Vol 153 (3) ◽  
pp. 1242-1255 ◽  
Author(s):  
Almudena Gómez-Hernández ◽  
Yolanda F. Otero ◽  
Natalia de las Heras ◽  
Óscar Escribano ◽  
Victoria Cachofeiro ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Vascular Dysfunction ◽  
Nuclear Factor Κb ◽  
Brown Fat ◽  
Visceral Adiposity ◽  
Inflammatory Activity ◽  
Nuclear Factor ◽  
Antibody Treatment ◽  
Tnf Α

In this study, we analyzed the role played by concerted expression of adipocytokines associated with brown fat lipoatrophy and increased visceral adiposity on triggering vascular insulin resistance and dysfunction in brown adipose tissue (BAT) insulin receptor knockout (BATIRKO) mice. In addition, we assessed whether vascular insulin resistance may aggravate vascular damage. The 52-wk-old, but not 33-wk-old, BATIRKO mice had a significant decrease of BAT mass associated with a significant increase of visceral white adipose tissue (WAT) mass, without changes in body weight. Brown fat lipoatrophy and increased visceral adiposity enhanced the concerted expression of adipocytokines (TNF-α, leptin, and plasminogen activator inhibitor 1) and nuclear factor-κB binding activity in BAT and visceral WAT, mainly in the gonadal depot, and aorta. Although those mice showed insulin sensitivity in the liver and skeletal muscle, insulin signaling in WAT (gonadal depot) and aorta was markedly impaired. Treatment with anti-TNF-α antibody impaired the inflammatory activity in visceral adipose tissue, attenuated insulin resistance in WAT and aorta and induced glucose tolerance. Finally, 52-wk-old BATIRKO mice showed vascular dysfunction, macrophage infiltration, oxidative stress, and a significant increase of gene markers of endothelial activation and inflammation, the latter effect being totally reverted by anti-TNF-α antibody treatment. Our results suggest that brown fat lipoatrophy and increased visceral adiposity through the concerted overexpression of cytoadipokines induces nuclear factor-κB-mediated inflammatory signaling, vascular insulin resistance, and vascular dysfunction. Inhibition of inflammatory activity by anti-TNF-α antibody treatment attenuates vascular insulin resistance and impairs gene expression of vascular dysfunction markers.

scholarly journals Adipocyte-specific Nos2 deletion improves insulin resistance and dyslipidemia through brown fat activation in diet-induced obese mice

2022 ◽  
pp. 101437
Author(s):  
Vanessa Rodrigues Vilela ◽  
Nolwenn Samson ◽  
Renato Nachbar ◽  
Lia Rossi Perazza ◽  
Gabriel Lachance ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Brown Fat ◽  
Obese Mice

scholarly journals Ubc9 Impairs Activation of the Brown Fat Energy Metabolism Program in Human White Adipocytes

2015 ◽  
Vol 29 (9) ◽  
pp. 1320-1333 ◽  
Author(s):  
Sean M. Hartig ◽  
David A. Bader ◽  
Kathleen V. Abadie ◽  
Massoud Motamed ◽  
Mark P. Hamilton ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Energy Storage ◽  
Energy Metabolism ◽  
Uncoupling Protein ◽  
Critical Role ◽  
Brown Fat ◽  
Negative Regulator ◽  
Brown Adipocyte ◽  
Uncoupling Protein 1

Abstract Insulin resistance and type 2 diabetes mellitus (T2DM) result from an inability to efficiently store and catabolize surplus energy in adipose tissue. Subcutaneous adipocytes protect against insulin resistance and T2DM by coupling differentiation with the induction of brown fat gene programs for efficient energy metabolism. Mechanisms that disrupt these programs in adipocytes are currently poorly defined, but represent therapeutic targets for the treatment of T2DM. To gain insight into these mechanisms, we performed a high-throughput microscopy screen that identified ubiquitin carrier protein 9 (Ubc9) as a negative regulator of energy storage in human sc adipocytes. Ubc9 depletion enhanced energy storage and induced the brown fat gene program in human sc adipocytes. Induction of adipocyte differentiation resulted in decreased Ubc9 expression commensurate with increased brown fat gene expression. Thiazolidinedione treatment reduced the interaction between Ubc9 and peroxisome proliferator-activated receptor (PPAR)γ, suggesting a mechanism by which Ubc9 represses PPARγ activity. In support of this hypothesis, Ubc9 overexpression remodeled energy metabolism in human sc adipocytes by selectively inhibiting brown adipocyte-specific function. Further, Ubc9 overexpression decreased uncoupling protein 1 expression by disrupting PPARγ binding at a critical uncoupling protein 1 enhancer region. Last, Ubc9 is significantly elevated in sc adipose tissue isolated from mouse models of insulin resistance as well as diabetic and insulin-resistant humans. Taken together, our findings demonstrate a critical role for Ubc9 in the regulation of sc adipocyte energy homeostasis.

269-OR: miR-409-3p Regulates Angiogenesis Brown Fat Adiposity and Insulin Resistance

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 269-OR
Author(s):  
DAKOTA R. BECKER-GREENE ◽  
HAO LI ◽  
WINONA WU ◽  
DENIZHAN OZDEMIR ◽  
IVANA HOLLAN ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Brown Fat

Characterization of insulin resistance and NIDDM in transgenic mice with reduced brown fat

Diabetes ◽  
1995 ◽  
Vol 44 (11) ◽  
pp. 1266-1273 ◽  
Author(s):  
A. Hamann ◽  
H. Benecke ◽  
Y. Le Marchand-Brustel ◽  
V. S. Susulic ◽  
B. B. Lowell ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Transgenic Mice ◽  
Brown Fat

scholarly journals Essential Role of IGFIR in the Onset of Male Brown Fat Thermogenic Function: Regulation of Glucose Homeostasis by Differential Organ-Specific Insulin Sensitivity

Endocrinology ◽  
2016 ◽  
Vol 157 (4) ◽  
pp. 1495-1511 ◽  
Author(s):  
Vanesa Viana-Huete ◽  
Carlos Guillén ◽  
Ana García-Aguilar ◽  
Gema García ◽  
Silvia Fernández ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Uncoupling Protein ◽  
High Plasma ◽  
Brown Fat ◽  
Severe Insulin Resistance ◽  
Brown Adipose ◽  
Total Fat

Abstract Brown fat is a thermogenic tissue that generates heat to maintain body temperature in cold environments and dissipate excess energy in response to overfeeding. We have addressed the role of the IGFIR in the brown fat development and function. Mice lacking IGFIR exhibited normal brown adipose tissue/body weight in knockout (KO) vs control mice. However, lack of IGFIR decreased uncoupling protein 1 expression in interscapular brown fat and beige cells in inguinal fat. More importantly, the lack of IGFIR resulted in an impaired cold acclimation. No differences in the total fat volume were found in the KO vs control mice. Epididymal fat showed larger adipocytes but with a lower number of adipocytes in KO vs control mice at age 12 months. In addition, KO mice showed a sustained moderate hyperinsulinemia and hypertriglyceridemia upon time and hepatic insulin insensitivity associated with lipid accumulation, with the outcome of a global insulin resistance. In addition, we found that the expression of uncoupling protein 3 in the skeletal muscle was decreased and its expression was increased in the heart in parallel with the expression of beta-2 adrenergic receptors. Upon nonobesogenic high-fat diet, we found a severe insulin resistance in the liver and in the skeletal muscle, but unchanged insulin sensitivity in the heart. In conclusion, our data suggest that IGFIR it is not an essential growth factor in the brown fat development in the presence of the IR and very high plasma levels of IGF-I, but it is indispensable for full brown fat functionality.

Characterization of Insulin Resistance and NIDDM in Transgenic Mice With Reduced Brown Fat

Diabetes ◽  
1995 ◽  
Vol 44 (11) ◽  
pp. 1266-1273 ◽  
Author(s):  
A. Hamann ◽  
H. Benecke ◽  
Y. L. Marchand-Brustel ◽  
V. S. Susulic ◽  
B. B. Lowell ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Transgenic Mice ◽  
Brown Fat

scholarly journals PO-178 Heat Treatment and Exercise Prevents Skeletal Muscle Insulin Resistance in Wistar Rats Fed High-Fat Diet

2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Jiexiu Zhao ◽  
Fei Qin ◽  
Minxiao Xu ◽  
Yanan Dong ◽  
Zhongwei Wang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Protein Expression ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Heat Exposure ◽  
Normal Diet ◽  
Brown Fat ◽  
Standard Diet ◽  
High Fat ◽  
Combined Exercise

Objective  Insulin resistance (IR) is associated with many related health complications. Previous studies demonstrate that heat and exercise independently reduce IR. The purpose of this study was to test the hypothesis that combined exercise and heating is even more favorable in reducing IR. Methods Male Wistar rats were randomly divided into five groups: exercise (NE; n=10), heated (HC; n=10), exercise and heated (HE; n=10), sedentary (NC; n=10), and normal diet plus sedentary (CC; n=10). All but the latter group was fed a high-fat diet (60% calories from fat) for 10 weeks while receiving heat and/or exercise exposure for latter 8 weeks. Following this regimen, protein expression from the soleus and extensor digitorum longus muscles, serum, and brown fat were analyzed using Western blotting. Results Exercise combined with heating shifted the metabolic characteristics of rats on a high-fat diet toward that observed in the rats on a standard diet. Specifically, eight weeks of combined heat and endurance exercise increased PGC-1α, CnA, CaMKIV and p38 MAPK protein expression in the soleus (P < 0.05), insulin protein expression in the serum (P < 0.05), and UCP1 protein expression in the brown fat (P < 0.05), when compared to the high fat fed sedentary group. There were some significant differences in responses (i.e., body weight and Leptin & Adiponectin concentrations) between the combined exercise and heat group relative to the exercise alone group. Conclusions  Exercise combined with heat exposure mitigates the development of IR, presumably from the Irisin pathway. The study provides potential non-pharmaceutical methods for therapeutic treatment of IR.

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