Abstract
The calcium activated cation channel transient receptor potential channel type M5 (TRPM5) is part of the downstream machinery of the taste receptors and have been shown to play a central role in taste signalling. In addition it is also found in other types of chemosensory cells in various parts of the body as well as in pancreatic β-cells. The aim of this study was to investigate the effects of TRPM5 gene ablation on body weight, insulin sensitivity and other metabolic parameters in long-term high caloric diet induced obesity. Trpm5 -/- mice gained significantly less body weight and fat mass on both palatable carbohydrate and fat rich cafeteria diet and 60% high fat diet (HFD) and developed less insulin resistance compared to wild type mice. A main finding was the clearly improved glucose tolerance in Trpm5 -/- mice compared to wild type mice on cafeteria diet, which was independent of body weight. In addition, it was shown that Trpm5 -/- mice consumed the same amount of calories when fed a HFD only or a HFD in combination with a palatable chocolate ball, which is in contrast to wild type mice that increased their caloric intake when fed the combination, mainly due to excessive consumption of the chocolate ball. Thus the palatable sugar containing diet induced overeating was prevented in Trpm5 -/- mice. This indicates that sweet taste induced overeating may be a cause for the increased energy intake and glucose intolerance development seen for wild type mice on a sugar and high fat rich cafeteria diet compared to when on a high fat diet. This study point to an important role for the taste signalling system and TRPM5 in diet induced glucose intolerance.
Highlights
The past decades have witnessed an epidemic in obesity, which is closely paralleled by an increase of type 2 diabetes [1,2]
We have showed that Trpm5-/- mice gained significantly less body weight and fat mass on both palatable carbohydrate rich cafeteria diet and 60% high fat diet (HFD) and were more glucose tolerant compared to wild type mice, which after cafeteria diet induced obesity was largely independent of body weight
In this study we show that Trpm5-/- mice gained significantly less body weight and fat mass on both palatable carbohydrate rich cafeteria diet and 60% HFD and were more glucose tolerant compared to wild type mice, which after cafeteria diet induced obesity was largely independent of body weight
Summary
The past decades have witnessed an epidemic in obesity, which is closely paralleled by an increase of type 2 diabetes [1,2]. Rodent studies have shown that unlimited access to high caloric diets leads to diet induced obesity and reduced insulin sensitivity and that diet induced obesity is due to several oral- (taste and texture) and post-oral (nutrient, energy content and activation of reward circuits) factors [10,11], as well as reduced energy expenditure Taste receptors such as T1R2/R3 (sweet receptor) and their downstream signalling machinery have attracted considerable attention in obesity and metabolism research because they contribute to oral evaluation of food by virtue of their expression in taste buds [12,13,14], and since they are present in enteroendocrine cells, thereby potentially contributing to post oral ingestive control and glucose homeostasis [15,16,17]. TRPM5 has been shown to be important for the release of endogenous Opioids from the duodenum [35]
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