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Disruption of the sugar-sensing receptor T1R2 attenuates metabolic derangements
associated with diet-induced obesity
#MMPMID26884387
Smith KR
; Hussain T
; Karimian Azari E
; Steiner JL
; Ayala JE
; Pratley RE
; Kyriazis GA
Am J Physiol Endocrinol Metab
2016[Apr]; 310
(8
): E688-E698
PMID26884387
show ga
Sweet taste receptors (STRs) on the tongue mediate gustatory sweet sensing, but
their expression in the gut, pancreas, and adipose tissue suggests a
physiological contribution to whole body nutrient sensing and metabolism.
However, little is known about the function and contribution of these sugar
sensors during metabolic stress induced by overnutrition and subsequent obesity.
Here, we investigated the effects of high-fat/low-carbohydrate (HF/LC) diet on
glucose homeostasis and energy balance in mice with global disruption of the
sweet taste receptor protein T1R2. We assessed body composition, energy balance,
glucose homeostasis, and tissue-specific nutrient metabolism in T1R2 knockout
(T1R2-KO) mice fed a HF/LC diet for 12 wk. HF/LC diet-fed T1R2-KO mice gained a
similar amount of body mass as did WT mice, but had reduced fat mass and
increased lean mass relative to WT mice. T1R2-KO mice were also hyperphagic and
hyperactive. Ablation of the T1R2 sugar sensor protected mice from HF/LC
diet-induced hyperinsulinemia and altered substrate utilization, including
increased rates of glucose oxidation and decreased liver triglyceride (TG)
accumulation, despite normal intestinal fat absorption. Finally, STRs (T1r2/T1r3)
were upregulated in the adipose tissue of WT mice in response to HF/LC diet, and
their expression positively correlated with fat mass and glucose intolerance. The
chemosensory receptor T1R2, plays an important role in glucose homeostasis during
diet-induced obesity through the regulation of yet to be identified molecular
mechanisms that alter energy disposal and utilization in peripheral tissues.
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