ACTH1-24 stimulates muscle cell glucose uptake

Area of Science:

• Endocrinology
• Cellular Physiology
• Metabolism

Background:

• Skeletal muscle is a primary site for glucose disposal.
• The role of hormones beyond insulin in regulating glucose uptake is an area of ongoing research.
• Adrenocorticotropic hormone (ACTH) is known for its effects on the adrenal cortex, but its direct effects on skeletal muscle glucose uptake are less understood.

Purpose of the Study:

• To investigate the effect of the N-terminal fragment of ACTH (ACTH1-24) on glucose uptake in rat skeletal muscle cells.
• To determine if ACTH1-24 modulates both basal and insulin-stimulated glucose uptake.
• To explore the mechanism of action of ACTH1-24 on glucose transport.

Main Methods:

• L6A-1 rat skeletal muscle cells were used.
• Cells were deprived of serum and insulin, then exposed to varying concentrations of ACTH1-24 in the presence of insulin.
• 3H-2-deoxyglucose (2-DG) uptake was measured.
• The effect of cytochalasin B, a glucose transporter inhibitor, was assessed.

Main Results:

• ACTH1-24 demonstrated a dose-dependent increase in 2-DG uptake (P < 0.001).
• This enhancement was observed in both basal and insulin-stimulated states.
• Cytochalasin B abolished the ACTH1-24-induced increase in glucose uptake, indicating involvement of glucose transporters.

Conclusions:

• ACTH1-24 stimulates carrier-mediated glucose uptake in skeletal muscle cells.
• The action of ACTH1-24 appears to be on the non-insulin mediated glucose uptake (NIMGU) system.
• ACTH1-24 may serve as a valuable tool for studying the NIMGU pathway.