Premium
Effects of gastric inhibitory polypeptide, glucagon‐like peptide‐1 and glucagon‐like peptide‐1 receptor agonists on Bone Cell Metabolism
Author(s) -
Hansen Morten S. S.,
Tencerova Michaela,
Frølich Jacob,
Kassem Moustapha,
Frost Morten
Publication year - 2018
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/bcpt.12850
Subject(s) - incretin , bone remodeling , glucose homeostasis , endocrinology , medicine , bone resorption , gastric inhibitory polypeptide , glucagon like peptide 1 , hormone , homeostasis , receptor , carbohydrate metabolism , glucagon , biology , insulin , type 2 diabetes , diabetes mellitus , insulin resistance
The relationship between gut and skeleton is increasingly recognized as part of the integrated physiology of the whole organism. The incretin hormones gastric inhibitory polypeptide ( GIP ) and glucagon‐like peptide‐1 ( GLP ‐1) are secreted from the intestine in response to nutrient intake and exhibit several physiological functions including regulation of islet hormone secretion and glucose levels. A number of GLP ‐1 receptor agonists ( GLP ‐1 RA s) are currently used in treatment of type 2 diabetes and obesity. However, GIP and GLP ‐1 cognate receptors are widely expressed suggesting that incretin hormones mediate effects beyond control of glucose homeostasis, and reports on associations between incretin hormones and bone metabolism have emerged. The aim of this MiniReview was to provide an overview of current knowledge regarding the in vivo and in vitro effects of GIP and GLP ‐1 on bone metabolism. We identified a total of 30 pre‐clinical and clinical investigations of the effects of GIP , GLP ‐1 and GLP ‐1 RA s on bone turnover markers, bone mineral density ( BMD ), bone microarchitecture and fracture risk. Studies conducted in cell cultures and rodents demonstrated that GIP and GLP ‐1 play a role in regulating skeletal homeostasis, with pre‐clinical data suggesting that GIP inhibits bone resorption whereas GLP ‐1 may promote bone formation and enhance bone material properties. These effects are not corroborated by clinical studies. While there is evidence of effects of GIP and GLP ‐1 on bone metabolism in pre‐clinical investigations, clinical trials are needed to clarify whether similar effects are present and clinically relevant in humans.