Dataset Information

Differential Effects of Diet and Weight on Taste Responses in Diet-Induced Obese Mice.

ABSTRACT: Objective: Previous studies have reported that individuals with obesity have reduced taste perception, but the relationship between obesity and taste is poorly understood. Earlier work has demonstrated that diet-induced obesity directly impairs taste. Currently, it is not clear whether these changes to taste are due to obesity or to the high-fat diet exposure. The goal of the current study was to determine whether diet or excess weight is responsible for the taste deficits induced by diet-induced obesity.

Methods: C57BL/6 mice were placed on either high-fat or standard chow in the presence or absence of captopril. Mice on captopril did not gain weight when exposed to a high-fat diet. Changes in the responses to different taste stimuli were evaluated using live cell imaging, brief-access licking, immunohistochemistry, and real-time polymerase chain reaction.

Results: Diet and weight gain each affected taste responses, but their effects varied by stimulus. Two key signaling proteins, α-gustducin and phospholipase Cβ2, were significantly reduced in the mice on the high-fat diet with and without weight gain, identifying a potential mechanism for the reduced taste responsiveness to some stimuli.

Conclusions: Our data indicate that, for some stimuli, diet alone can cause taste deficits, even without the onset of obesity.

SUBMITTER: Ahart ZC

PROVIDER: S-EPMC6981059 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature

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Differential Effects of Diet and Weight on Taste Responses in Diet-Induced Obese Mice.

Ahart Zachary C ZC Martin Laura E LE Kemp Bailey R BR Dutta Banik Debarghya D Roberts Stefan G E SGE Torregrossa Ann-Marie AM Medler Kathryn F KF

Obesity (Silver Spring, Md.) 20191231 2

<h4>Objective</h4>Previous studies have reported that individuals with obesity have reduced taste perception, but the relationship between obesity and taste is poorly understood. Earlier work has demonstrated that diet-induced obesity directly impairs taste. Currently, it is not clear whether these changes to taste are due to obesity or to the high-fat diet exposure. The goal of the current study was to determine whether diet or excess weight is responsible for the taste deficits induced by diet ...[more]

PMID: 31891242

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Project description:BackgroundNon-alcoholic fatty liver disease (NAFLD) ranks first among liver diseases in Western countries. NAFLD is typically associated with obesity and diabetes, however it also develops in lean individuals without metabolic syndrome. The prevalence of lean NAFLD is 7 percent in the U.S. and 25-30 percent in some Asian countries. NAFLD starts with excess liver fat accumulation (NAFL), progresses to nonalcoholic steatohepatitis (NASH), cirrhosis and hepatocellular carcinoma (HCC). The pathogenesis of lean NASH-HCC and how it differs from obese NASH-HCC is not well understood.MethodsIn this work, we generated a mouse model of lean and obese NASH-HCC using a choline deficient/high trans-fat/fructose/cholesterol diet and a choline supplemented/high trans-fat/fructose/cholesterol diet, respectively, to compare progression to NASH-HCC in lean versus obese mice. Comparisons were made at the organismal, histological, and molecular level by investigating fatty acid metabolism in the plasma of these mice.ResultsObese mice showed more pronounced glucose intolerance and insulin resistance, higher levels of plasma cholesterol and triglycerides, and higher penetrance of NASH compared to lean mice. Despite the abnormal metabolic profile of obese mice, male obese and lean mice developed HCC with similar penetrance (53.3% and 53.8%, respectively), albeit lean mice showed faster tumor progression as evidenced by the larger tumor size and lower HCC-free survival. None of the female lean mice developed HCC, while 50% of female obese mice developed HCC. Both groups of mice showed a reduction in plasma polyunsaturated fatty acids (PUFAs), however, the levels were higher towards the endpoint in obese mice compared to lean mice.ConclusionsUnhealthy diet composition appears to drive progression to NASH-HCC rather than the organismal effects of obesity. PUFA levels may increase due to systemic inflammation in obese mice and act as suppressors of tumor progression, thus delaying HCC progression in obese mice compared to lean mice. These models could be used to further dissect the molecular pathogenesis of lean and obese NASH-HCC and address the mechanisms whereby PUFAs may be implicated in hepatocarcinogenesis.

Project description:BackgroundIntermittent severe energy restriction is popular for weight management. To investigate whether intermittent moderate energy restriction may improve this approach by enhancing weight loss efficiency, we conducted a study in mice, where energy intake can be controlled.MethodsMale C57/Bl6 mice that had been rendered obese by an ad libitum diet high in fat and sugar for 22 weeks were then fed one of two energy-restricted normal chow diets for a 12-week weight loss phase. The continuous diet (CD) provided 82% of the energy intake of age-matched ad libitum chow-fed controls. The intermittent diet (ID) provided cycles of 82% of control intake for 5-6 consecutive days, and ad libitum intake for 1-3 days. Weight loss efficiency during this phase was calculated as (total weight change) ÷ [(total energy intake of mice on CD or ID)-(total average energy intake of controls)]. Subsets of mice then underwent a 3-week weight regain phase involving ad libitum re-feeding.ResultsMice on the ID showed transient hyperphagia relative to controls during each 1-3-day ad libitum feeding period, and overall ate significantly more than CD mice (91.1±1.0 versus 82.2±0.5% of control intake respectively, n = 10, P<0.05). There were no significant differences between CD and ID groups at the end of the weight loss or weight regain phases with respect to body weight, fat mass, circulating glucose or insulin concentrations, or the insulin resistance index. Weight loss efficiency was significantly greater with ID than with CD (0.042±0.007 versus 0.018±0.001 g/kJ, n = 10, P<0.01). Mice on the CD exhibited significantly greater hypothalamic mRNA expression of proopiomelanocortin (POMC) relative to ID and control mice, with no differences in neuropeptide Y or agouti-related peptide mRNA expression between energy-restricted groups.ConclusionIntermittent moderate energy restriction may offer an advantage over continuous moderate energy restriction, because it induces significantly greater weight loss relative to energy deficit in mice.

Dataset Information

Differential Effects of Diet and Weight on Taste Responses in Diet-Induced Obese Mice.

Publications

Differential Effects of Diet and Weight on Taste Responses in Diet-Induced Obese Mice.

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