TRPM5 in the battle against diabetes and obesity

Abstract

TRPM5 is a non-selective monovalent cation channel activated by increases in intracellular Ca . It has a distinct expression pattern: expression is detected in chemosensitive tissues from solitary chemosensory cells to the taste receptor cells and in pancreatic β-cells. The role of TRPM5 has been investigated with the use of knockout mouse models. Trpm5 mice have a lack of type II taste perception and show reduced glucose-induced insulin secretion. Expression levels of TRPM5 are reduced in obese, leptin-signalling-deficient mice, and mutations in TRPM5 have been associated with type II diabetes and metabolic syndrome. In this review, we aim to give an overview of the activation, selectivity, modulation and physiological roles of TRPM5.

The Dynamic Effects of Isosteviol on Insulin Secretion and Its Inability to Counteract the Impaired β-Cell Function during Gluco-, Lipo-, and Aminoacidotoxicity: Studies In Vitro

“…This may be because ISV influences a receptor (e.g., a TRPM5-related receptor) and remains bound for some time, resulting in the effect gradually disappearing. TRPM5, transient receptor potential cation channel subfamily melastatin member 5, is a monovalent cation channel located in various human cells, including Type II taste receptor cells and pancreatic β-cells [ 48 , 49 , 50 ]. An increase in intracellular calcium would activate TRPM5; Philippaert K. et al (2017) proved that the potentiation of the channel’s activity by steviol glycosides modulates taste responses and insulin release, which would explain the feature of the compound being sweet and lowering blood glucose concurrently [ 51 ].…”

Adipose tissue—more than just fat

“…A number of articles addressing basic mechanisms related to obesity have recently appeared in Acta physiologica. [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] One area of clinical relevance for obese patients is the immune system. Duan et al 20 recapitulate the connections between a high-fat diet and diseases.…”

“…Mutations in the non-selective monovalent cation channel TRPM5 have been associated with type II diabetes and metabolic syndrome. 18 In addition, CD36, a mediator for fatty acid uptake in skeletal muscle, was identified as a link between obesity and skeletal muscle redox homeostasis and muscle regeneration. 19 When Verpoorten et al fed mice with a high-fat diet, the CD36 deficient group occurred to be protected from weight-gain in comparison to the wild-type mice.…”

Obesity, adipocytes and insulin resistance—Friends for life?

“…This receptor is expressed on pancreatic β‐cells and type 2 taste receptor cells. TRPM5‐ko mice show reduced weight gain and food intake during a high‐fat diet, mainly by impaired tasting of sweetness . TRPM5 activation could furthermore provoke insulin secretion and prevention of diabetes type 2, but results from animal studies need to be transferred to human obesity.…”