Tailgate Study: A Pilot Study Measuring the Impact of Food and Alcohol Intake on Whole‐body and Liver Metabolism

Elevated liver fat is associated with hyperglycemia, hyperlipidemia, and insulin resistance, especially in overweight individuals. Excess food intake and alcohol can each increase intrahepatic lipid yet, the two are commonly consumed together. Few studies have assessed the combined effects of overeating and excess alcohol intake, both of which stimulate hepatic de novo lipogenesis (DNL) and have the potential to increase intrahepatic TG (IHTG). The purpose of the present study was to investigate a single bout of hypercaloric intake, including alcohol, to mimic energy intake typically occur during a tailgate event. METHODS Three days prior to the study, subjects consumed D2O (50 ml deuterated water twice daily) to label DNL. Males, n=15 (age 29.8±6.1y (mean±SD), BMI 32.2±6.2) completed a 5‐hour inpatient study in which fasting and fed‐state measurements were made. A breathalyzer was used every 30 minutes to maintain breath alcohol concentrations (BAC) between ~0.08–0.10 g/dL. Changes in blood concentrations of glucose, insulin, NEFA, and TG were measured enzymatically; IHTG was evaluated by MRI (n=12). Body composition was assessed by DEXA. The morning following the study, substrate oxidation was measured via indirect calorimetry. TG‐rich lipoproteins (TRL‐TG) were isolated by ultracentrifugation and fatty acids methyl esters analyzed by GC/MS; DNL was calculated using Mass Isotopomer Distribution Analysis. RESULTS The total amount of food consumed during the 5h period was 4990±545 kcal, of which 34% of energy was from carbohydrate (CHO), 37% fat, 10% protein, and 19% alcohol. Alcohol intake was 137±25 g/subject over 5h which resulted in an average BAC of 0.08±0.01 g/dL. Energy consumption significantly increased TRL‐TG by 3‐fold (61 to 281 mg/dL, P <0.0001) and absolute DNL by 8‐fold (5.6 to 50.8 mg/dL, P <0.0001, Fig. 1). Glucose increased modestly (91 to 112 mg/dL, P <0.0001), yet insulin was elevated by 6‐fold (10 to 76 μU/mL, P =0.005). Surprisingly, no changes were observed in IHTG (8.4±6.3 to 8.5±6.8 %, P =0.945). The morning following the study, fasting glucose concentrations were normal (93±9 mg/dL); however, the respiratory quotient (RQ) was 0.93±0.08, reflecting elevated tissue glucose oxidation. Correlation analysis revealed that in the fasting state, absolute DNL was significantly associated with visceral adipose tissue (r=0.583, P =0.036). Fasting IHTG was related to aspartate aminotransferase (r=0.763, P =0.003), HOMA‐IR (r=0.707, P =0.008), and body fat (r=0.775, P =0.002). During the study, a higher absolute DNL AUC correlated with the amount of CHO consumed (r=0.619, P =0.019) and tended to be related to BAC (r=0.490, P =0.089). The absolute DNL AUC measured on the study day predicted fasting RQ the next morning (r=0.832, P =0.0004) and glucose oxidation rates (r=0.845, P =0.0003). A negative relationship between fed DNL and fat oxidation was observed (r= −0.796, P =0.001, Fig. 2) which occurred as a result of an RQ>1 in six subjects indicating net fat synthesis the next morning. CONCLUSION These data suggest that acute overconsumption of CHO may impact DNL more than excess alcohol. In overweight, otherwise healthy men, the excess energy intake was accommodated without increasing IHTG. The combination of excess energy and alcohol led to metabolic changes that may further exacerbate weight gain by extending the duration of elevated DNL through the next day. Support or Funding Information University of Missouri This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .