Adipose Tissue Dysregulation and Reduced Insulin Sensitivity in Non-Obese Individuals with Enlarged Abdominal Adipose Cells

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Adipose Tissue Dysregulation and Reduced Insulin Sensitivity in Non-Obese Individuals with Enlarged Abdominal Adipose Cells

Show simple item record Hammarstedt, Ann Graham, Timothy E Kahn, Barbara 2013-04-22T19:32:17Z 2012
dc.identifier.citation Hammarstedt, Ann, Timothy E. Graham, and Barbara Kahn. 2012. Adipose tissue dysregulation and reduced insulin sensitivity in non-obese individuals with enlarged abdominal adipose cells. Diabetology & Metabolic Syndrome 4:42. en_US
dc.identifier.issn 1758-5996 en_US
dc.description.abstract Background: Obesity contributes to Type 2 diabetes by promoting systemic insulin resistance. Obesity causes features of metabolic dysfunction in the adipose tissue that may contribute to later impairments of insulin action in skeletal muscle and liver; these include reduced insulin-stimulated glucose transport, reduced expression of GLUT4, altered expression of adipokines, and adipocyte hypertrophy. Animal studies have shown that expansion of adipose tissue alone is not sufficient to cause systemic insulin resistance in the absence of adipose tissue metabolic dysfunction. To determine if this holds true for humans, we studied the relationship between insulin resistance and markers of adipose tissue dysfunction in non-obese individuals. Method 32 non-obese first-degree relatives of Type 2 diabetic patients were recruited. Glucose tolerance was determined by an oral glucose tolerance test and insulin sensitivity was measured with the hyperinsulinaemic-euglycaemic clamp. Blood samples were collected and subcutaneous abdominal adipose tissue biopsies obtained for gene/protein expression and adipocyte cell size measurements. Results: Our findings show that also in non-obese individuals low insulin sensitivity is associated with signs of adipose tissue metabolic dysfunction characterized by low expression of GLUT4, altered adipokine profile and enlarged adipocyte cell size. In this group, insulin sensitivity is positively correlated to GLUT4 mRNA (R = 0.49, p = 0.011) and protein (R = 0.51, p = 0.004) expression, as well as with circulating adiponectin levels (R = 0.46, 0 = 0.009). In addition, insulin sensitivity is inversely correlated to circulating RBP4 (R = −0.61, 0 = 0.003) and adipocyte cell size (R = −0.40, p = 0.022). Furthermore, these features are inter-correlated and also associated with other clinical features of the metabolic syndrome in the absence of obesity. No association could be found between the hypertrophy-associated adipocyte dysregulation and HIF-1alpha in this group of non-obese individuals. Conclusions: In conclusion, these findings support the concept that it is not obesity per se, but rather metabolic dysfunction of adipose tissue that is associated with systemic insulin resistance and the metabolic syndrome. en_US
dc.language.iso en_US en_US
dc.publisher BioMed Central en_US
dc.relation.isversionof doi:10.1186/1758-5996-4-42 en_US
dc.relation.hasversion en_US
dash.license LAA
dc.subject Adipocyte cell size en_US
dc.subject BMI en_US
dc.subject Insulin sensitivity en_US
dc.subject GLUT4 en_US
dc.subject Adiponectin en_US
dc.subject RBP4 en_US
dc.title Adipose Tissue Dysregulation and Reduced Insulin Sensitivity in Non-Obese Individuals with Enlarged Abdominal Adipose Cells en_US
dc.type Journal Article en_US
dc.description.version Version of Record en_US
dc.relation.journal Diabetology & Metabolic Syndrome en_US Kahn, Barbara 2013-04-22T19:32:17Z

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