GH regulates important physiological processes, including somatic growth and development, and carbohydrate and lipid metabolism. GH deficiency and GH replacement therapy exert opposite effects on body composition and fat accumulation, suggesting that GH may directly regulate adipocyte functions. Multiple studies have shown that in tissues previously deprived of GH, short-term stimulation with GH is able to mimic the actions of insulin, including stimulation of amino-acid and glucose transport, and lipogenesis. However, the antagonistic effects of GH on insulin-mediated metabolic responses are well-documented: GH excess in patients with GH-producing pituitary tumors causes hyperinsulinemia, insulin resistance, and even clinical diabetes mellitus. These apparently contradictory effects may be explained at the molecular level by the complex interplay between GH and insulin signaling. In this review, we examine the consequences of acute and chronic effects of GH on visceral fat and on metabolic responses in adipocytes, and discuss experimental data illustrating the integrated crosstalk between GH and insulin.