GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
The positive effects of growth hormone-releasing peptide-6 on weight gain and fat mass accrual depend on the insulin/glucose status.
Granado. Miriam M; García-Cáceres. Cristina C; Frago. Laura M LM; Argente. Jesús J; Chowen. Julie A JA
Key Findings
- GHRP‑6 alone did not improve hyperglycemia, hyperphagia, or weight loss in diabetic rats.
- Insulin alone corrected blood sugar, reduced hunger signals, and normalized hypothalamic neuropeptide expression.
- Combining GHRP‑6 with insulin led to greater weight gain, increased visceral fat, larger adipocytes, and higher leptin than either treatment alone.
Practical Outcomes
- For biohackers, GHRP‑6 may only promote weight or fat gain when insulin levels are elevated, such as after carbohydrate‑rich meals or with supplemental insulin. To avoid unwanted fat accumulation, consider timing GHRP‑6 away from high‑insulin states; conversely, if the goal is mass gain, pairing it with carbs or insulin‑boosting strategies could enhance its effect.
Summary
In diabetic rats, the growth‑hormone‑releasing peptide GHRP‑6 only helped increase weight and belly fat when insulin was also present. GHRP‑6 alone didn’t fix high blood sugar or weight loss, but together with insulin it boosted appetite, fat‑cell size, and leptin levels. This suggests GHRP‑6’s fat‑gaining effects depend on having enough insulin or glucose in the body.
Abstract
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.
Study Information
pubmed
2010
2010-03-10T00:00:00.000Z
10.1210/en.2009-1394
10
61