Methylglyoxal impairs β-adrenergic signalling in primary rat adipocytes

Abstract

Methylglyoxal (MG) is dicarbonyl aldehyde generated intracellularly from glucose and from some other compounds. Its increased formation is associated with several harmful consequences. In the present study, short-term effects of MG on metabolism of isolated rat adipocytes were determined. Insulin-induced lipogenesis was unchanged by MG. However, epinephrine-stimulated lipolysis was shown to be significantly reduced in adipocytes exposed to 200 µM MG. This inhibitory effect was similar in the presence of low and high concentrations of glucose, and also in the presence of alanine. However, MG failed to affect lipolysis induced by forskolin (activator of adenylate cyclase), dibutyryl-cAMP (activator of PKA) and DPCPX (adenosine A₁ receptor antagonist). It was also revealed that lipolysis was unchanged by MG in fat cells pre-incubated with this compound, and then stimulated with epinephrine alone. Our results suggest that MG may impair β-adrenergic signalling in rat adipocytes due to interaction with epinephrine, and thereby disturbs lipolysis.

Keywords:

• Adipocytes
• methylglyoxal
• metabolism

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

Research conducted by the statutory funding No. 506.558.04.00 of the Faculty of Veterinary Medicine and Animal Science Poznan University of Life Sciences, Poland; Department of Animal Physiology and Biochemistry.