The prevalence of pediatric obesity has increased over the past 40 years and the prevalence in 6 to 19 years old is currently over 20%. This increase in obesity is predicted to negatively impact health and result in multiple obesity-related comorbidities in adulthood. Taste and food preferences are complex, and understanding the potential driving factors is essential, particularly due to the rise in obesity and obesity-related illnesses worldwide. Previous studies assessing taste preference and eating patterns have demonstrated an association between single nucleotide polymorphisms (SNPs) at taste receptor genes and fat taste sensitivity (CD36), sweet taste preference (TAS1R2), and bitter taste aversion (TAS2R38). Therefore, the goal of the current study was to investigate the intersection of genotype (rs1761667 of CD36, rs35874116 of TAS1R2 and rs713598 of TAS2R38) and phenotypic diet intake and quality in female and male adolescents. Genotype was determined by allelic discrimination assay in children 10-16 years of age (females, n=167 and males, n=145) enrolled in the Translational Investigation of Growth and Everyday Routines in Kids (TIGER Kids) Study. Anthropometrics and 24-hour dietary recalls were conducted for each participant and Healthy Eating Index (HEI) scores, a measure of diet quality (lower scores suggest lower diet quality), were calculated. The effect of sex and genetic variation was assessed using a two-way ANOVA. Based on allelic discrimination assays, the expression rates of CD36 AA/AG/GG, TAS1R2 TT/CT/CC and TAS2R38 CC/CG/GG did not differ between females and males. Preliminary results indicate that adolescents with CD36 GG and TAS2R38 CG have higher BMI percentiles compared to other genotypes ( p<.05). The TAS2R38 genotype was associated with HEI-sodium, HEI-total protein, and HEI-whole grain ( p<.05). Adolescents with TAS2R38 CC had the lowest HEI-sodium and HEI-total protein scores and adolescents with TAS2R38 CG had the lowest HEI-whole grain scores. An interaction between sex and TAS2R38 genotype was detected for HEI-fatty acids and HEI-total score ( p<.05). Males with TAS2R38 CG had the lowest HEI-fatty acids and HEI-total scores, females with TAS2R38 GG had the lowest HEI-fatty acids score and females with TAS2R38 CG had the lowest HEI-total score. CD36 and TAS1R2 genotypes were associated with HEI-dairy, with adolescents with CD36 CG and those with TAS1R2 CT having the lowest scores ( p<.05). The TAS1R2 genotype was associated with HEI-fatty acids, with adolescents with TAS1R2 TT having the lowest score ( p<.05). Fat and sugar intake (g) were positively correlated in SNPs associated with altered fat perception ( CD36 AA) in males, and sugar intake ( TAS1R2 TT) and overall energy intake ( TAS2R39 CC) in females ( p<.05). In males and females with the CD36 GG genotype, fat intake was positively correlated with sugar intake ( p<.05), supporting the finding of a higher BMI percentile in adolescents with this genotype. Overall, the results from these analyses support the intersection between sex and genetic variation on HEI and suggest that SNPs in taste receptor genes differentially affect diet quality in adolescent males and females. Further understanding of the role of taste receptor SNPs on food choices and diet quality is needed to better tailor dietary interventions in the pediatric population. USDA 3092-51000-056-04A. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Chronic alcohol consumption is the most common and costly form of substance abuse in the United States and is highly prevalent in persons living with HIV (PLWH). Combination antiretroviral therapy (ART) has significantly increased longevity in PLWH and over 50% of PLWH in the U.S.A. are 50 years of age or older. Aging, unhealthy alcohol use and increased survival of PLWH on ART are complicated by metabolic dysregulation. The goal of the current study was to test the hypothesis that unhealthy alcohol use in PLWH increases the prevalence of dysglycemia following an oral glucose tolerance test (OGTT). Participants with a fasting blood glucose (FBG) of 94–125mg/dL (n=105) were recruited from a cohort of in‐care PLWH (≥ 18 years) enrolled in the ongoing translational study, New Orleans Alcohol Use in HIV (NOAH) and from the Greater New Orleans area. Alcohol use was determined by the Alcohol Use Disorders Identification Test (AUDIT). An AUDIT score ≥ 5 was defined as unhealthy alcohol use (n=47) versus an AUDIT score of < 5 (n=52). Questionnaires (i.e. AUDIT and Timeline Followback) and Phosphatidylethanol (PEth) were used to further describe and confirm alcohol use. All participants underwent an OGTT, which included an assessment of plasma glucose 2 hours following consumption of a standard glucose solution (75g, Trutol). Circulating insulin, c‐peptide and adiponectin were measured. Anthropometric measurements included assessment of weight, Body Mass Index, and waist/hip ratio (WHR). Among participants with an impaired FBG, 44.8% exhibited unhealthy alcohol use. 2‐h plasma glucose values were positively correlated with AUDIT, PEth and 2‐h insulin levels and there was a moderate, but not statistically significant (p = 0.06) increase in 2‐h plasma glucose levels following OGTT in participants with unhealthy alcohol use. AUDIT was also positively correlated with Timeline Followback (grams of alcohol) and PEth values, supporting the use of AUDIT as a valid marker of alcohol use. WHR, which is indicative of abdominal obesity, and has been linked to a higher incidence of insulin resistance, was higher in participants with unhealthy alcohol use and was positively correlated with FBG. Based on the results from the OGTT, participants were divided into 3 categories, Normal (2‐h glucose <140mg/dL), Prediabetic (140–199mg/dL) and Diabetic (≥200mg/dL). Of the participants with Normal plasma glucose, 37.3% exhibited unhealthy alcohol use. Among Prediabetics, 70.6% exhibited unhealthy alcohol use and in Diabetics, 80% exhibited unhealthy alcohol use. Unhealthy alcohol use (AUDIT ≥5) was associated with a 4.13 odds ratio (1.54, 11.08) of being Prediabetic or Diabetic. Overall, these data support our hypothesis that in PLWH with impaired fasting glucose, unhealthy alcohol use is associated with dysglycemia following an OGTT. These results suggest that directed interventions that focus on glucose regulation and alcohol use, including aerobic exercise, could have a profound impact on ameliorating the risk of developing metabolic comorbidities in this population of at‐risk PLWH. Support or Funding Information NIH NIAAA UH2AA026198 to PEM
The inability to switching between fuel sources (fat and carbohydrates), termed metabolic inflexibility, plays a prominent role in the development of type 2 diabetes and obesity. Evidence suggests that chronic exercise interventions and weight reduction improve metabolic flexibility (MF). However, little is known about the impact of a single bout of high-intensity interval exercise (HIIE) on MF. PURPOSE: To assess the impact that HIIE has on MF and blood flow in response to a mixed meal tolerance test (MMTT) performed without exercise (BL) or following 1H or 48H post-HIIE. METHODS: Participants (n=16, aged 21.2 ± 1.2 y, BMI 22.6 ± 2.7 kg/m2) completed 3 mixed meal tolerance tests (MMTT; 412.2 ± 71.5 kcal) (BL, 1H and 48H) lasting 180 minutes. Indirect calorimetry measurements were taken prior to the mixed meal (0 min), 60 min, and 120 min post mixed meal. MF was determined by subtracting RER 60 min - RER 0 min and analyzing the rate of carbohydrate and fat oxidation/suppression (FatOx). HIIE was 10 x 60s intervals at 90% (154.6 ± 35.6 W) of power output achieved at VO2peak, followed by 60s of recovery. Additionally, we measured blood flow in the vastus lateralis (VL) every 30-min utilizing near-infrared spectroscopy (NIRS). RESULTS: Fasting FATox was elevated 48H post-exercise compared to BL (1.31 ± 0.39 mg/kg/min vs.0.96 ± 0.32 mg/kg/min, p=0.04). The ability to suppress FATox at the 60-min time-point of the MMTT was significantly higher 48H post-exercise compared to BL (~20% vs. ~12%, p=0.01). Increased VL blood flow was detected 120-minutes into the MMTT during BL. When compared to BL, 1H post-exercise VL blood flow changes were significantly higher at 60 (1.8 fold, p=0.03) and 120-min (2.0 fold, p=0.04) time points. CONCLUSIONS: Our results suggest, a single bout of HIIE improves MF up to 48H post-exercise, which is characterized by higher fasting and meal-induced suppression of FATox. Postprandial VL blood flow was also stimulated to a greater degree 1H post-exercise when compared to the BL postprandial measurement. The impact of acute HIIE demonstrates MF can be improved acutely, prior to chronic adaptations. Supported By NIH Grant T32 AT 004094 Funded in part by a College of Human Sciences and Education Dean’s Circle Grant
The current experiment tested the hypothesis that consumption of a high-fat diet (HFD) would differentially affect metabolic parameters in obesity-prone Osborne-Mendel (OM) and obesity-resistant S5B/Pl (S5B) rats. In OM rats consuming a HFD, an increase in HFD intake, body mass, and percent fat mass, and a HFD-induced decrease in metabolic rate and energy expenditure were demonstrated. In S5B rats consuming a HFD, no change in percent body fat or HFD intake was demonstrated and HFD increased metabolic rate and energy expenditure. To assess whether HFD differentially altered skeletal muscle markers of metabolism in OM and S5B rats, the expression of the transporters, CD36 and GLUT4, and the energy sensors, AMPK and PPARγ, in the gastrocnemius muscle was measured. Oxidation and lipid accumulation in the gastrocnemius muscle was histologically determined. Consumption of a HFD decreased phosphorylated AMPK and PPARγ expression in the skeletal muscle of obesity-prone OM rats. Lipid accumulation in skeletal muscle was significantly higher in OM rats fed a HFD. Overall, these data suggest that the differential response to HFD on metabolic rate, energy expenditure, and phosphorylated AMPK and PPARγ in OM and S5B rats, may partially account for differences in the susceptibility to develop obesity.
