Metabolic complications are common in treated HIV patients. Their etiology is multifactorial and the development of increased abdominal fat contributes to cardiovascular risk and impaired quality of life. Treated patients with fat mass distribution changes have relative growth hormone deficiency. Both pharmacologic and physiologic doses of growth hormone reduce the increased visceral adipose tissue and improve the associated abnormal lipid profiles in short-term studies. However, impaired glucose homeostasis changes and significant musculoskeletal toxicity occurs. A novel growth hormone-releasing factor analogue, tesamorelin, provides a physiologic means of restoring a normal growth hormone secretion profile and reduces increased visceral adipose tissue, improving both abnormal lipid profiles and patients' quality of life. Glucose homeostasis is generally well maintained. Cessation of treatment with either growth hormone or tesamorelin results in a prompt return of truncal obesity. Management strategies for the long-term maintenance of the reduced visceral adipose tissue have not yet been clarified and long-term effects on decreasing cardiovascular risks and improving clinical outcomes are uncertain.