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Chronic Ethanol-Induced Insulin Resistance Is Associated With Macrophage Infiltration Into Adipose Tissue and Altered Expression of Adipocytokines
- Source :
- Alcoholism: Clinical and Experimental Research. 31:1581-1588
- Publication Year :
- 2007
- Publisher :
- Wiley, 2007.
-
Abstract
- Background: Chronic ethanol consumption disrupts glucose homeostasis and is associated with the development of insulin resistance. While adipose tissue and skeletal muscle are the two major organs utilizing glucose in response to insulin, the relative contribution of these two tissues to impaired glucose homeostasis during chronic ethanol feeding is not known. As other models of insulin resistance, such as obesity, are characterized by an infiltration of macrophages into adipose tissue, as well as changes in the expression of adipocytokines that play a central role in the regulation of insulin sensitivity, we hypothesized that chronic ethanol-induced insulin resistance would be associated with increased macrophage infiltration into adipose tissue and changes in the expression of adipocytokines by adipose tissue. Methods: Male Wistar rats were fed a liquid diet containing ethanol as 36% of calories or pair-fed a control diet for 4 weeks. The effects of chronic ethanol feeding on insulin-stimulated glucose utilization were studied using the hyperinsulinemic-euglycemic clamp technique, coupled with the use of isotopic tracers. Further, macrophage infiltration into adipose tissue and expression of adipocytokines were also assessed after chronic ethanol feeding. Results: Hyperinsulinemic-euglycemic clamp studies revealed that chronic ethanol feeding to rats decreased whole-body glucose utilization and decreased insulin-mediated suppression of hepatic glucose production. Chronic ethanol feeding decreased glucose uptake in epididymal, subcutaneous, and omental adipose tissue during the hyperinsulinemic-euglycemic clamp, but had no effect on glucose disposal in skeletal muscle. Chronic ethanol feeding increased the infiltration of macrophages into epididymal adipose tissue and changed the expression of mRNA for adipocytokines: expression of mRNA for monocyte chemoattractant protein 1, tumor necrosis factor α, and interleukin-6 were increased, while expression of mRNA for retinol binding protein 4 and adiponectin were decreased in epididymal adipose tissue. Conclusions: These data demonstrate that chronic ethanol feeding results in the development of insulin resistance, associated with impaired insulin-mediated suppression of hepatic glucose production and decreased insulin-stimulated glucose uptake into adipose tissue. Chronic ethanol-induced insulin resistance was associated with increased macrophage infiltration into adipose tissue, as well as changes in the expression of adipocytokines by adipose tissue.
- Subjects :
- Male
medicine.medical_specialty
Glucose uptake
Adipose tissue macrophages
Medicine (miscellaneous)
Adipose tissue
White adipose tissue
Biology
Toxicology
Insulin resistance
Cell Movement
Internal medicine
medicine
Animals
Glucose homeostasis
Rats, Wistar
Muscle, Skeletal
Chemokine CCL2
Ethanol
Adiponectin
Interleukin-6
Tumor Necrosis Factor-alpha
Macrophages
Central Nervous System Depressants
Glucose clamp technique
medicine.disease
Rats
Retinol-Binding Proteins
Alcoholism
Disease Models, Animal
Psychiatry and Mental health
Glucose
Endocrinology
Adipose Tissue
Glucose Clamp Technique
Cytokines
Insulin Resistance
Retinol-Binding Proteins, Plasma
Subjects
Details
- ISSN :
- 15300277 and 01456008
- Volume :
- 31
- Database :
- OpenAIRE
- Journal :
- Alcoholism: Clinical and Experimental Research
- Accession number :
- edsair.doi.dedup.....06842b29cc0c27d23910dc4aaac7b5f9