Peptide-YY3-36/glucagon-like peptide-1 combination treatment of obese diabetic mice improves insulin sensitivity associated with recovered pancreatic β-cell function and synergistic activation of discrete hypothalamic and brainstem neuronal circuitries

Brandon B Boland,Rhianna C Laker, Siobhan O'Brien, Sadichha Sitaula,Isabelle Sermadiras,Jens Christian Nielsen,Pernille Barkholt,Urmas Roostalu,Jacob Hecksher-Sørensen, Sara Rubek Sejthen,Ditte Dencker Thorbek,Arthur Suckow, Nicole Burmeister,Stephanie Oldham,Sarah Will,Victor G Howard,Benji M Gill, Philip Newton,Jacqueline Naylor,David C Hornigold,Jotham Austin,Louise Lantier,Owen P McGuinness,James L Trevaskis,Joseph S Grimsby,Christopher J Rhodes

Molecular Metabolism（2022）

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摘要

•Long-acting Peptide-YY3-36 + Glucagon-Like Peptide-1 therapy induces weight loss and T2D remission in obese/diabetic mice.•Fc-PYY3-36 + Fc-GLP-1 enhances endogenous pancreatic β-cell functional recovery.•Improved insulin sensitivity independent of weight loss was seen following Fc-PYY3-36 + Fc-GLP-1 treatment.•Fc-PYY3-36 + Fc-GLP-1 synergistically trigger discrete hypothalamic and brainstem nuclei of the CNS.

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关键词

Diabetes,Obesity,Insulin sensitivity,Pancreatic β-cell,Hypothalamus,Glucagon-like peptide-1 (GLP-1),Peptide-YY3-36 (PYY3-36),Diabetes remission,Central nervous system,Glucose homeostasis

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