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GPR41 and GPR43 modulate rodent pancreatic α-cell function and growth.

A Sánchez-Roncero1, T Fernández-Marcelo2, A A Pérez-Serna3

  • 1Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío, CSIC, Departamento de Fisiología Médica y Biofísica, Universidad de Sevilla, Sevilla, Spain.

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Short-chain fatty acid receptors GPR41 and GPR43 activate glucagon secretion in alpha cells, offering a potential therapeutic target for type 2 diabetes (T2D) and hyperglucagonemia.

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Glucagon secretionIsletsShorth-chain fatty acidsType 2 diabetesgpr41gpr43

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Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Cell Biology

Background:

  • Short-chain fatty acid (SCFA) receptors GPR41 and GPR43 are known to regulate insulin secretion from beta cells.
  • Their specific roles in alpha cells, particularly in the context of hyperglucagonemia observed in type 2 diabetes (T2D), remain largely unexplored.
  • Understanding these roles is crucial for developing targeted T2D therapies.

Purpose of the Study:

  • To investigate the function of GPR41 and GPR43 in pancreatic alpha cells.
  • To determine if synthetic agonists for GPR41 and GPR43 can modulate alpha cell physiology and glucagon secretion under various metabolic conditions.
  • To explore the therapeutic potential of targeting these receptors for managing T2D-related glycemic dysregulation.

Main Methods:

  • Utilized alphaTC1.9 cell lines and primary rat islets to study SCFA receptor roles.
  • Investigated glucagon expression and secretion under high-fat diet (HFD)-induced insulin resistance and lactation models.
  • Employed specific GPR41 (AR420626) and GPR43 ((S)-2-(4-chlorophenyl)-3,3-dimethyl-N-(5-phenylthiazol-2-yl) butanamide) agonists to elucidate mechanisms.

Main Results:

  • GPR41 and GPR43 were confirmed to be localized within alpha cells of pancreatic islets.
  • Treatment with GPR41 and GPR43 agonists increased glucagon (Gcg) expression and secretion, particularly at low glucose concentrations.
  • High-fat diet induced glucose intolerance, hyperglucagonemia, and enhanced islet Gpr41/43 expression, with agonists further increasing Gcg expression in HFD islets.

Conclusions:

  • GPR41 and GPR43 agonists modulate alpha cell function, increasing glucagon secretion.
  • GPR41 activation in lactating rats promoted Gcg expression and alpha cell replication via Gαi.
  • GPR41 presents a promising therapeutic target for hyperglucagonemia and glycemic control in T2D.