Browsing by Subject "food intake"

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    Enhancing hepatic mitochondrial fatty acid oxidation stimulates eating in food-deprived mice
    (APS, 2015-01) Mansouri, Abdelhak; Pacheco-López, Gustavo; Ramachandran, Deepti; Arnold, Myrtha; Leitner, Claudia; Prip-Buus, Carina; Langhans, Wolfgang; Morral, Núria; Department of Medical & Molecular Genetics, IU School of Medicine
    Hepatic fatty acid oxidation (FAO) has long been implicated in the control of eating. Nevertheless, direct evidence for a causal relationship between changes in hepatic FAO and changes in food intake is still missing. Here we tested whether increasing hepatic FAO via adenovirus-mediated expression of a mutated form of the key regulatory enzyme of mitochondrial FAO carnitine palmitoyltransferase 1A (CPT1mt), which is active but insensitive to inhibition by malonyl-CoA, affects eating and metabolism in mice. CPT1mt expression increased hepatocellular CPT1 protein levels. This resulted in an increase in circulating ketone body levels in fasted CPT1mt-expressing mice, suggesting an increase in hepatic FAO. These mice did not show any significant changes in cumulative food intake, energy expenditure, or respiratory quotient after 4-h food deprivation. After 24-h food deprivation, however, the CPT1mt-expressing mice displayed increased food intake. Thus expression of CPT1mt in the liver increases hepatic FAO capacity, but does not inhibit eating. Rather, it may even stimulate eating after prolonged food deprivation. These data do not support the hypothesis that an increase in hepatic FAO decreases food intake.
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    Ghrelin is not Related to Hunger or Calories Consumed at Breakfast in Lean and Obese Women
    (Office of the Vice Chancellor for Research, 2015-04-17) Morgan, Rachel C.; Acton, Anthony J.; Armstrong, Cheryl L.H.; Eiler, William J.A.; Case, K. Rose; Soeurt, Christina M.; Dzemidzic, Mario; Kareken, David A.; Considine, Robert V.
    Background: The mechanisms that result in greater caloric intake in obese individuals are incompletely understood. Ghrelin administration increases ad lib food intake in humans. We investigated the relationship of ghrelin to calorie consumption and hunger at breakfast on two separate occasions in lean and obese women. Methods: 23 lean (BMI 22.3±0.5 kg/m2, 26.5±1.0 yr) and 25 obese (BMI 36.9±0.7 kg/m2, 27.8±1.1 yr) women participated in a noncontiguous 2 day study. The minimum and maximum days between visits were 6 and 43 days. Participants were given the same breakfast on both days (turkey sausage, French toast with margarine/syrup, fruit cup, coffee, tea, diet soda, or water) with portions adjusted to provide 20% of the daily energy requirement for weight maintenance. Subjects were instructed to eat until full. Hunger was evaluated on a Satiety Labeled Intensity Magnitude Scale (SLIM) before and after the meal. Anchors were “greatest imaginable fullness” at 0 and “greatest imaginable hunger” at 100. Blood samples were collected over 120 minutes for measurement of active ghrelin. Results: Lean subjects consumed an equivalent number of calories on both days (380.0±14.6 vs 378.2±14.9 kcal), as did the obese (419.4±16.2 vs 428.8±15.4 kcal). On average for both days, obese consumed significantly more breakfast calories than lean (424.1±11.1 vs 379.1±10.3 kcal; P<0.01), but the same percentage of calories provided (85.7±1.8 vs 86.1±1.7 %kcal). Lean subjects rated hunger before breakfast the same on both days (69.2±1.6 vs 71.7±1.4), as did the obese (69.8±1.6 vs 69.6±1.8), and there was no difference between the groups. Lean subjects rated hunger after breakfast the same on both days (27.8±1.9 vs 30.3±2.4), as did the obese (25.0±1.7 vs 24.3±1.8). The reduction in hunger score following breakfast was significant for both groups (P<0.0001), with the obese reporting significantly less hunger/more fullness after breakfast than the lean (P=0.02). Fasting ghrelin was significantly greater in the lean than obese women (549.9±58.9 vs 231.0±29.1 pg/ml; P<0.0001). Ghrelin was significantly reduced at 60 min following breakfast in the lean (375.8±49.2 pg/ml; P=0.028) but not the obese (212.2±26.4 pg/ml). Ghrelin was not related to hunger score prior to breakfast, and there was no relationship between reduction in ghrelin and hunger score in the lean or obese. Conclusion: Caloric intake (as a percentage provided) and hunger scores before breakfast on two occasions were the same for both lean and obese women. Fasting ghrelin was significantly different between lean and obese women but did not predict hunger score or calories consumed. Our findings do not support a role for ghrelin in driving food intake at breakfast.