Viewpoints on the Way to the Consensus Session: Where does insulin resistance start? The adipose tissue

FA overflow from adipocytes to skeletal muscle and other tissues may result in free radical formation during oxidative phosphorylation, the intramyocellular accumulation of triglyceride, and the production of toxic lipid metabolites (fatty-acyl CoAs, diacylglycerol, and ceramides) and metabolic inte...

Full description

Saved in:
Bibliographic Details
Published inDiabetes care Vol. 32; no. 11; pp. S168 - S173
Main Author Iozzo, Patricia
Format Journal Article
LanguageEnglish
Published United States American Diabetes Association 01.11.2009
Subjects
Adipokines - physiology
Adipose Tissue - physiopathology
Adipose tissues
Body fat
Cannabinoid Receptor Modulators - physiology
Causes of
Consensus
Demographic aspects
Diabetes Mellitus, Type 2 - physiopathology
Diabetes Progression, Prevention, and Treatment
Fatty Acids - metabolism
Fatty Acids - pharmacology
Glucocorticoids - physiology
Health aspects
Heart - drug effects
Heart - physiopathology
Humans
Hyperglycemia
Inflammation - physiopathology
Insulin resistance
Insulin Resistance - physiology
Liver - drug effects
Liver - physiopathology
Metabolic diseases
Metabolic disorders
Nutrition
Obesity - physiopathology
Risk factors
Italy
Online AccessGet full text

Cover

More Information
Summary:FA overflow from adipocytes to skeletal muscle and other tissues may result in free radical formation during oxidative phosphorylation, the intramyocellular accumulation of triglyceride, and the production of toxic lipid metabolites (fatty-acyl CoAs, diacylglycerol, and ceramides) and metabolic intermediates, which reflect oxidative damage (4), both of which can interfere with the insulin signaling cascade. [...] fat-specific insulin resistance appears to be an early and irreversible defect that can explain the causal relationship between adipocyte dysfunction, extra-adipose tissue (i.e. , muscle and liver), and insulin resistance.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
ObjectType-Review-3
ISSN:0149-5992
1935-5548
1935-5548
DOI:10.2337/dc09-S304