Amelioration

of diet-induced diabetes mellitus by removal za NIC zil m.u (epididymal and perinephric) fat removal. All groups were submitted to evaluation of basal glucose and insulin levels and in DIO mice. After visceral fat removal the levels of adipokines returned to near control levels. The present include the impaired suppression of hepatic glucose pro-production of glycerol (Williamson et al. 1966), and abnormal 1999, Kim et al. 1999) and one model of aging (Gabriely et al. longer be appropriately tyrosine-phosphorylated in response resistance, visceral adiposity, hyperinsulinemia, and impaired 699Journal of Endocrinology (2006) 191, 699–7062002). Themetabolic consequences of visceral fat removal were associated with improved hepatic insulin action (Barzilai et al. insulin signal transduction. As an attempt to further characterize the role played by visceral fat in the development DOI: 10.1677/joe.1.07069production of adipose tissue-derived hormones and cyto-kines, such as tumour necrosis factor (TNF)-a, interleukin (IL)-1b, IL-6, leptin, adiponectin, and resistin (Hotamisligil et al. 1996, Steppan et al. 2001). Recent studies have shown that the removal of visceral fat reverses insulin resistance in twomodels of obesity (Barzilai et al. to an incoming insulin signal. As a result, the activation of downstream effectors of the insulin signaling pathway is hampered (Hotamisligil 2000, 2003). In a recent study, we characterized an animal model of diet-induced obesity (DIO) that rapidly becomes diabetic (De Souza et al. 2005b). This animal model presents insulinduction (O’Shaughnessy et al. 1995), increased portal release of free fatty acids (Bjorntorp 1990), increased visceral I kappa kinase (IKK) (Hotamisligil 2003, Barreiro et al. 2004). Once serine-phosphorylated, proteins such as the insulin receptor, insulin receptor-substrate (IRS)-1 and IRS-2 can nowas evaluated by immunoprecipitation and immunoblot, and serum adipokine levels were determined by ELISA. DIO mice became diabetic (228 versus 115 mg/dl), hyperinuli-nemic (7.59 versus 3.15 ng/ml) and insulin resistant (Kitt 2.88 versus 4.97%/min) as compared with control. Visceral fa