scholarly journals Brown adipose tissue–specific insulin receptor knockout shows diabetic phenotype without insulin resistance

2001 ◽  
Vol 108 (8) ◽  
pp. 1205-1213 ◽  
Author(s):  
Carmen Guerra ◽  
Paloma Navarro ◽  
Angela M. Valverde ◽  
Monica Arribas ◽  
Jens Brüning ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Insulin Receptor ◽  
Tissue Specific ◽  
Brown Adipose ◽  
Specific Insulin

scholarly journals Brown adipose tissue–specific insulin receptor knockout shows diabetic phenotype without insulin resistance

2019 ◽  
Vol 129 (1) ◽  
pp. 437-437 ◽  
Author(s):  
Carmen Guerra ◽  
Paloma Navarro ◽  
Angela M. Valverde ◽  
Monica Arribas ◽  
Jens Brüning ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Insulin Receptor ◽  
Tissue Specific ◽  
Brown Adipose ◽  
Specific Insulin

Guarana supplementation attenuated obesity, insulin resistance, and adipokines dysregulation induced by a standardized human Western diet via brown adipose tissue activation

2019 ◽  
Vol 33 (5) ◽  
pp. 1394-1403 ◽  
Author(s):  
Rafael Calixto Bortolin ◽  
Amanda Rodrigues Vargas ◽  
Vitor Ramos ◽  
Juciano Gasparotto ◽  
Paloma Rodrigues Chaves ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Western Diet ◽  
Brown Adipose

scholarly journals Tissue-specific insulin resistance in mice with mutations in the insulin receptor, IRS-1, and IRS-2

2000 ◽  
Vol 105 (2) ◽  
pp. 199-205 ◽  
Author(s):  
Yoshiaki Kido ◽  
Deborah J. Burks ◽  
Dominic Withers ◽  
Jens C. Bruning ◽  
C. Ronald Kahn ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Receptor ◽  
Tissue Specific ◽  
Specific Insulin

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.

Fat feeding causes widespread in vivo insulin resistance, decreased energy expenditure, and obesity in rats

1986 ◽  
Vol 251 (5) ◽  
pp. E576-E583 ◽  
Author(s):  
L. H. Storlien ◽  
D. E. James ◽  
K. M. Burleigh ◽  
D. J. Chisholm ◽  
E. W. Kraegen
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Metabolic Rate ◽  
Brown Adipose Tissue ◽  
Whole Body ◽  
Brown Adipose ◽  
Glucose Output ◽  
Fat Feeding

High levels of dietary fat may contribute to both insulin resistance and obesity in humans but evidence is limited. The euglycemic clamp technique combined with tracer administration was used to study insulin action in vivo in liver and individual peripheral tissues after fat feeding. Basal and nutrient-stimulated metabolic rate was assessed by open-circuit respirometry. Adult male rats were pair-fed isocaloric diets high in either carbohydrate (69% of calories; HiCHO) or fat (59% of calories; HiFAT) for 24 +/- 1 days. Feeding of the HiFAT diet resulted in a greater than 50% reduction in net whole-body glucose utilization at midphysiological insulin levels (90-100 mU/l) due to both reduced glucose disposal and, to a lesser extent, failure to suppress liver glucose output. Major suppressive effects of the HiFAT diet on glucose uptake were found in oxidative skeletal muscles (29-61%) and in brown adipose tissue (BAT; 78-90%), the latter accounting for over 20% of the whole-body effect. There was no difference in basal metabolic rate but thermogenesis in response to glucose ingestion was higher in the HiCHO group. In contrast to their reduced BAT weight, the HiFAT group accumulated more white adipose tissue, consistent with reduced energy expenditure. HiFAT feeding also resulted in major decreases in basal and insulin-stimulated conversion of glucose to lipid in liver (26-60%) and brown adipose tissue (88-90%) with relatively less effect in white adipose (0-43%). We conclude that high-fat feeding results in insulin resistance due mainly to effects in oxidative skeletal muscle and BAT.(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document