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Leg Fat Deposits Predict Insulin Resistance in the Metabolic Syndrome Patients,

Peripheral fat, unlike central fat, may offer protection against insulin resistance and atherosclerotic risk in healthy populations. Hyperinsulinemia is a critical component of the metabolic syndrome and contributes to the increased the risk of cardiac disease. While overall obesity is an established determinant of insulin resistance, the contribution of regional(leg) fat to metabolic abnormalities is unclear.

Recent data suggest that peripheral fat, unlike central fat, may offer protection against insulin resistance and atherosclerotic risk in healthy populations, but the relationship of visceral, subcutaneous and leg fat to insulin resistance has not been investigated in patients with the metabolic syndrome.

We evaluated 26 (13 male and 15 female) subjects with the metabolic syndrome as defined by WHO criteria, and an age-matched group of 40 controls without metabolic syndrome. Abdominal subcutaneous and visceral fat were determined by cross-sectional CT scanning and peripheral extremity fat by DXA. Insulin resistance was assessed by HOMA.

In contrast, in the healthy controls only VAT ( =0.05, p< 0.01) was positively associated with HOMA and accounted for only 28% of the variance in insulin resistance. Our data suggest that VAT is a significant determinant of insulin resistance in healthy subjects.

Complicated interactions exist between regional fat depots that contribute to insulin action in subjects with the metabolic syndrome, in whom SAT, the VAT:SAT ratio and leg fat independently predict insulin resistance.

These data are the first to demonstrate that increased extremity fat, in contrast to SAT and VAT, protects against insulin resistance in a strictly defined population with the metabolic syndrome. Strategies to alter fat distribution may improve metabolic abnormalities in patients with the metabolic syndrome.

L Elizabeth Bernstein, Sunnie Kim, Jaqueline Berry, Dolan Sara, Polyxeni Koutkia, Steven Grinspoon. Prog of Nutrit Metab and Neuroendocrine Unit, Massachusetts Gen Hosp, Boston, MA

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DID YOU KNOW: The Incretin mimetics Glucagon-Like Peptide 1 (7-36) Amide (GLP-1) and Exendin-4 Inhibit Dopamine and Norepinephrine Uptake in the Hypothalamus and this seems to play a satiety role after both peripheral and central administration. Given the role played by catecholamine in central modulation of feeding, we can conclude that the central anorectic effects of GLP-1 and exendin-4 could be partially mediated by inhibited uptake of DA and NE in the hypothalamus.

Brunetti L, Michelotto B, Orlando G, Vacca Central Nervous System & Gut Regulatory Peptides ENDO 2005