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The present article discusses how accumulation of triacylglycerol in adipocytes can lead to deterioration of the responsiveness of glucose metabolism in other tissues. Lipodystrophy, lack of adipose tissue, is also associated with insulin resistance. Any plausible explanation for the link between excess adipose tissue and insulin resistance needs to be able to account for this observation. Adipose tissue in obesity becomes refractory to suppression of fat mobilization by insulin, and also to the normal acute stimulatory effect of insulin on activation of lipoprotein lipase (involved in fat storage). The net effect is as though adipocytes are \u2018full up\u2019 and resisting further fat storage. Thus, in the postprandial period especially, there is an excess flux of circulating lipid metabolites that would normally have been \u2018absorbed\u2019 by adipose tissue. This situation leads to fat deposition in other tissues. Accumulation of triacylglycerol in skeletal muscles and in liver is associated with insulin resistance. In lipodystrophy there is insufficient adipose tissue to absorb the postprandial influx of fatty acids, so these fatty acids will again be directed to other tissues. This view of the link between adipose tissue and insulin resistance emphasises the important role of adipose tissue in \u2018buffering\u2019 the daily influx of dietary fat entering the circulation and preventing excessive exposure of other tissues to this influx.<\/jats:p>","DOI":"10.1079\/pns200195","type":"journal-article","created":{"date-parts":[[2008,9,29]],"date-time":"2008-09-29T17:41:44Z","timestamp":1222710104000},"page":"375-380","source":"Crossref","is-referenced-by-count":162,"title":["Adipose tissue and the insulin resistance syndrome"],"prefix":"10.1017","volume":"60","author":[{"given":"Keith 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