Obesity is the Western World’s most common health problem, and has reached epidemic proportions according to the World Health Organisation. More than 20% of the adult population in developed countries are obese – more than 300 million adults worldwide. In addition, more than 50% of adults in developed countries are overweight. Obesity is associated with other health-related problems such as heart disease, cancer and diabetes.

Amongst its metabolic effects, hGH can induce inhibition of lipoprotein lipase activity in adipose tissue, stimulating lipolysis in adipocytes, which results in the reduction of fat cell mass [4-7]. Moreover, a correlation has been found between adiposity and the reduced circulating levels of hGH [8]. When applied systemically, hGH reduces body fat mass and influences fat distribution [9]. Therefore, treatment with hGH should theoretically have a positive impact on obesity. However, long term treatment with hGH is associated with various health risks, including glucose intolerance and insulin resistance, diabetes, acromegaly, cancer, edema, and hypertension [10-13].

There is the potential for the side effects associated with use of growth hormone when growth hormone secretagogues are used, particularly if the use is not under medical supervision. There are limited data on the safety of intravenous and subcutaneous use of AOD-9604 and on the long-term oral use of AOD-9604 in doses in excess of those used in clinical trials.

Ghrelin and GH secretagogues, including GH-releasing peptide (GHRP)-6, stimulate food intake and adiposity. Because insulin modulates the hypothalamic response to GH secretagogues and acts synergistically with ghrelin on lipogenesis in vitro, we analyzed whether insulin plays a role in the metabolic effects of GHRP-6 in vivo. Streptozotocin-induced diabetic rats received saline, GHRP-6, insulin, or insulin plus GHRP-6 once daily for 8 wk. Rats receiving saline suffered hyperglycemia, hyperphagia, polydipsia, and weight loss. Insulin, but not GHRP-6, improved these parameters (P < 0.001 for all), as well as the diabetes-induced increase in hypothalamic mRNA levels of neuropeptide Y and agouti-related peptide and decrease in proopiomelanocortin. Cocaine amphetamine-related transcript mRNA levels were also reduced in diabetic rats, with GHRP-6 inducing a further decrease (P < 0.03) and insulin an increase. Diabetic rats receiving insulin plus GHRP-6 gained more weight and had increased epididymal fat mass and serum leptin levels compared with all other groups (P < 0.001). In epididymal adipose tissue, diabetic rats injected with saline had smaller adipocytes (P < 0.001), decreased fatty acid synthase (FAS; P < 0.001), and glucose transporter-4 (P < 0.001) and increased hormone sensitive lipase (P < 0.001) and proliferator-activated receptor-gamma mRNA levels (P < 0.01). Insulin normalized these parameters to control values. GHRP-6 treatment increased FAS and glucose transporter-4 gene expression and potentiated insulin's effect on epididymal fat mass, adipocyte size (P < 0.001), FAS (P < 0.001), and glucose transporter-4 (P < 0.05). In conclusion, GHRP-6 and insulin exert an additive effect on weight gain and visceral fat mass accrual in diabetic rats, indicating that some of GHRP-6's metabolic effects depend on the insulin/glucose status.
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