GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Effect of desacyl ghrelin, obestatin and related peptides on triglyceride storage, metabolism and GHSR signaling in 3T3-L1 adipocytes.
Miegueu. Pierre P; St Pierre. David D; Broglio. Fabio F; Cianflone. Katherine K
Key Findings
- GHRP‑6 (and acyl‑ghrelin) increased pre‑adipocyte proliferation up to 200% in vitro.
- All tested peptides, including GHRP‑6, enhanced differentiation of pre‑adipocytes into adipocytes (up to 300%).
- GHRP‑6 raised fatty‑acid uptake in mature adipocytes, while glucose transport stayed the same.
- GHSR1 signaling pathways (blocked by specific antagonists) mediate the fatty‑acid uptake effect.
Practical Outcomes
- For biohackers using GHRP‑6 to boost growth hormone, be aware it may also promote fat‑cell growth and fatty‑acid storage, which could counter leanness goals. The findings are from cell‑culture work, so any real‑world impact is uncertain and likely dose‑ and timing‑dependent. Consider monitoring body‑fat changes if you combine GHRP‑6 with other protocols.
Summary
The study shows that GHRP‑6, like other ghrelin‑related peptides, can directly make fat‑cell precursors multiply and turn into mature fat cells, and it boosts the cells' ability to take up fatty acids. It doesn’t change glucose uptake, but it may help store more fat. These effects were seen in mouse cell cultures, not in people.
Abstract
Acyl-ghrelin (AG), desacyl-ghrelin (DAG) and obestatin are all derived from the same gene transcript; however their plasma levels do not necessarily change in parallel. The influence of these peptides towards the development of obesity and their direct effects on adipocyte physiology has not been thoroughly investigated. This study was designed to evaluate the direct effects of peptides of the ghrelin family on preadipocyte proliferation, differentiation and adipocyte lipid and glucose metabolism in 3T3-L1 cells. 3T3 cells were treated with physiological peptide concentrations for 1 h to 9 days, and the relevant assays measured. In preadipocytes, AG, GHRP-6 and DAG stimulated proliferation, measured as (3)H-thymidine incorporation (up to 200%, P < 0.05), while all peptides stimulated differentiation (up to 300%, P < 0.01) as compared to standard differentiation conditions. In adipocytes, FA uptake was increased in a concentration-dependent manner especially with obestatin (three- to fourfold, P < 0.001) and DAG (three- to fivefold, P < 0.001). By contrast, glucose transport was unchanged. DAG and obestatin significantly decreased lipolysis measured as non-esterified fatty acid and glycerol release by 50%, P < 0.05-0.01 and 51%, P < 0.01, respectively. Interestingly, DAG stimulation of FA uptake was blocked with GHSR1 antagonist (D-lys(3))-GHRP-6 (P < 0.05), phospholipase C inhibitor U73122 and phosphatidylinositol-3-kinase inhibitor wortmannin (P < 0.001). Finally, in omental but not subcutaneous human adipose tissue, GHSR1 correlated with BMI (r = 0.549, P < 0.05) and insulin (r = 0.681, P < 0.01). Taken together, these results suggest that ghrelin-related peptides may directly affect adipose tissue metabolism.
Study Information
pubmed
2011
2011-02-01T00:00:00.000Z
10.1002/jcb.22983
82
51