Published online Jan 15, 2018. doi: 10.4239/wjd.v9.i1.25
Peer-review started: February 12, 2017
First decision: May 17, 2017
Revised: November 17, 2017
Accepted: December 4, 2017
Article in press: December 4, 2017
Published online: January 15, 2018
To study complete dose-dependent effects of obestatin on lipolytic and glucose transport activities in human adipocyte preparations highly responsive to insulin.
Adipocytes were prepared by liberase digestion from subcutaneous abdominal adipose tissue obtained from overweight subjects undergoing plastic surgery. The index of lipolytic activity was the glycerol released in the incubation medium, while glucose transport was assessed by [3H]-2-deoxyglucose uptake assay.
When tested from 0.1 nmol/L to 1 μmol/L, obestatin did not stimulate glycerol release; it did not inhibit the lipolytic effect of isoprenaline and did not alter the insulin antilipolytic effect. Obestatin hardly activated glucose transport at 1 μmol/L only. Moreover, the obestatin stimulation effect was clearly lower than the threefold increase induced by insulin 100 nmol/L.
Low doses of obestatin cannot directly influence lipolysis and glucose uptake in human fat cells.
Core tip: We have compared in adipocytes the well-known glucose uptake stimulation and lipolysis inhibition induced by insulin to the effects of obestatin, a gut peptide derived from ghrelin gene recently proposed to act on fat cells. Obestatin was much less efficient than insulin in adipocytes from human abdominal subcutaneous adipose tissue. Indeed, obestatin weakly activated hexose transport while it could not reproduce the antilipolytic effect of insulin at any tested concentration. We therefore propose that obestatin does not rapidly modulate lipogenesis and lipolysis and that its contribution to energy homeostasis depends on actions other than a direct control of adipocyte metabolism.