Control of food intake by fatty acid oxidation

1986 ◽  
Vol 250 (6) ◽  
pp. R1003-R1006 ◽  
Author(s):  
E. Scharrer ◽  
W. Langhans
Keyword(s):  
Fatty Acid ◽  
Blood Glucose ◽  
Food Intake ◽  
Fatty Acid Oxidation ◽  
Ketone Bodies ◽  
Acid Oxidation ◽  
Dark Phase ◽  
Fat Level ◽  
Plasma Ffa

The role of fatty acid oxidation in the control of food intake was studied using mercaptoacetate (MA), an inhibitor of fatty acid oxidation. Food intake, plasma free fatty acids (FFA) and ketone bodies, and blood glucose were measured. Rats were fed either a low-fat (LF, 3.33% fat) or a medium-fat (MF, 18% fat) diet. At the onset of the dark phase of the lighting cycle, MA did not affect food intake in LF rats but increased it 74% in MF rats in comparison to control. Four hours after the injection the effect of MA on food intake disappeared. In the middle of the bright phase of the lighting cycle, MA increased food intake in MF rats approximately 120% up to 6 h postinjection. After MA, plasma FFA concentration was elevated, and plasma 3-hydroxybutyrate concentration was lowered, indicating that fatty acid oxidation had been successfully reduced. MA did not affect blood glucose. These results indicate fatty acid oxidation is involved in the control of food intake, at least when the dietary fat level is relatively high.

Role of fatty acid oxidation in food intake and hunger motivation in Syrian hamsters

1988 ◽  
Vol 43 (5) ◽  
pp. 617-623 ◽  
Author(s):  
Jill E. Schneider ◽  
Sandra J. Lazzarini ◽  
Mark I. Friedman ◽  
George N. Wade
Keyword(s):  
Fatty Acid ◽  
Food Intake ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Syrian Hamsters ◽  
Hunger Motivation

scholarly journals The effects of inhibition of fatty acid oxidation in suckling newborn rats

1977 ◽  
Vol 166 (3) ◽  
pp. 631-634 ◽  
Author(s):  
J P Pégorier ◽  
P Ferré ◽  
J Girard
Keyword(s):  
Fatty Acid ◽  
Blood Glucose ◽  
Fatty Acid Oxidation ◽  
Glucose Utilization ◽  
Ketone Bodies ◽  
Normal Blood ◽  
Acid Oxidation ◽  
Newborn Rats ◽  
Normal Blood Glucose ◽  
Blood Ketone Bodies

Inhibition of fatty acid oxidation with pent-4-enoate in suckling newborn rats caused a fall in blood [glucose] and blood [ketone bodies] and inhibition of gluconeogenesis from lactate. Glucose utilization was not increased in newborn rats injected with pent-4-enoate. Active fatty acid oxidation appears to be essential to support gluconeogenesis and to maintain normal blood [glucose] in suckling newborn rats.

Mating behavior is controlled by acute changes in metabolic fuels

2002 ◽  
Vol 282 (3) ◽  
pp. R782-R790 ◽  
Author(s):  
Jennifer L. Temple ◽  
Jill E. Schneider ◽  
Deanna K. Scott ◽  
Alexander Korutz ◽  
Emilie F. Rissman
Keyword(s):  
Fatty Acid ◽  
Blood Glucose ◽  
Mating Behavior ◽  
Fatty Acid Oxidation ◽  
Food Restriction ◽  
Ketone Bodies ◽  
Acid Oxidation ◽  
Glucose Levels ◽  
Ad Libitum ◽  
Feeding Bout

Mild food restriction for 48 h inhibits mating behavior in female musk shrews ( Suncus murinus). However, mating behavior is restored after a 90-min feeding bout. In this series of experiments, we examined the role of metabolic fuels in this behavioral restoration. First, drugs reported to block glycolysis or fatty acid oxidation were given 2 h before mating. Both treatments inhibited mating in food-restricted females that were refed after treatment. Blood glucose levels were assessed in females that were fed ad libitum, food restricted, or food restricted and refed for 90 min. Food restriction significantly lowered blood glucose compared with ad libitum feeding or food restriction in combination with 90 min of refeeding. However, neither glucose nor fat alone could substitute for food and promote mating behavior in food-restricted females. In addition, analysis of ketone bodies and body composition in females demonstrated low or undetectable levels of these energy substrates. Our data suggest that musk shrews have relatively little stored energy. Therefore, female musk shrews rely on continuous food intake and monitor multiple cues acutely, including glucose availability and fatty acid oxidation. This ensures that mating does not occur when adequate energy is unavailable.

Meal composition affects postprandial fatty acid oxidation

1993 ◽  
Vol 264 (6) ◽  
pp. R1065-R1070 ◽  
Author(s):  
D. M. Surina ◽  
W. Langhans ◽  
R. Pauli ◽  
C. Wenk
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Nutrient Utilization ◽  
Whole Body ◽  
Acid Oxidation ◽  
Plasma Ffa ◽  
Hepatic Fatty Acid Oxidation ◽  
Beta Hydroxybutyrate ◽  
Chain Fatty Acids

The influence of macronutrient content of a meal on postprandial fatty acid oxidation was investigated in 13 Caucasian males after consumption of a high-fat (HF) breakfast (33% carbohydrate, 52% fat, 15% protein) and after an equicaloric high-carbohydrate (HC) breakfast (78% carbohydrate, 6% fat, 15% protein). The HF breakfast contained short- and medium-chain fatty acids, as well as long-chain fatty acids. Respiratory quotient (RQ) and plasma beta-hydroxybutyrate (BHB) were measured during the 3 h after the meal as indicators of whole body substrate oxidation and hepatic fatty acid oxidation, respectively. Plasma levels of free fatty acids (FFA), triglycerides, glucose, insulin, and lactate were also determined because of their relationship to nutrient utilization. RQ was significantly lower and plasma BHB was higher after the HF breakfast than after the HC breakfast, implying that more fat is burned in general and specifically in the liver after an HF meal. As expected, plasma FFA and triglycerides were higher after the HF meal, and insulin and lactate were higher after the HC meal. In sum, oxidation of ingested fat occurred in response to a single HF meal.

Effect of Age and Dietary Fat Level on Fatty Acid Oxidation in the Neonatal Pig

1978 ◽  
Vol 108 (10) ◽  
pp. 1621-1634 ◽  
Author(s):  
Ronald G. Wolfe ◽  
Charles V. Maxwell ◽  
Eldon C. Nelson
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Dietary Fat ◽  
Acid Oxidation ◽  
Fat Level ◽  
Neonatal Pig ◽  
Effect Of Age

scholarly journals Reduced Liver-Specific PGC1a Increases Susceptibility for Short-Term Diet-induced Weight Gain in Male Mice

2020 ◽  
Author(s):  
E. Matthew Morris ◽  
Roberto D. Noland ◽  
Michael E. Ponte ◽  
Michelle L. Montonye ◽  
Julie A. Christianson ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Weight Gain ◽  
Energy Metabolism ◽  
Energy Balance ◽  
Fatty Acid Oxidation ◽  
Positive Energy ◽  
Acid Oxidation ◽  
Male Mice ◽  
Short Term

AbstractCentral integration of peripheral neural signals is one mechanism by which systemic energy homeostasis is regulated. Previous work described increased acute food intake following chemical reduction of hepatic fatty acid oxidation and ATP levels, which was prevented by common hepatic branch vagotomy (HBV). However, possible offsite actions of the chemical compounds confound the precise role of liver energy metabolism. Herein, we used a liver-specific PGC1a heterozygous (LPGC1a) mouse model, with associated reductions in mitochondrial fatty acid oxidation and respiratory capacity, to assess the role of liver energy metabolism in systemic energy homeostasis. LPGC1a male mice have 70% greater high-fat/high-sucrose (HFHS) diet-induced weight gain and 35% greater positive energy balance compared to wildtype (WT) (p<0.05). The greater energy balance was associated with altered feeding behavior and lower activity energy expenditure during HFHS in LPGC1a males. Importantly, no differences in HFHS-induced weight gain or energy metabolism was observed between female WT and LPGC1a mice. WT and LPGC1a mice underwent sham or HBV to assess whether vagal signaling was involved in HFHS-induced weight gain of male LPGC1a mice. HBV increased HFHS-induced weight gain (85%, p<0.05) in male WT, but not LPGC1a mice. As above, sham LPGC1a males gain 70% more weight during short-term HFHS feeding than sham WT (p<0.05). These data demonstrate a sexspecific role of reduced liver energy metabolism in acute diet-induced weight gain, and the need of more nuanced assessment of the role of vagal signaling in short-term diet-induced weight gain.Key Points SummaryReduced liver PGC1a expression results in reduced mitochondrial fatty acid oxidation and respiratory capacity in male mice.Male mice with reduced liver PGC1a expression (LPGC1a) demonstrate greater short-term high-fat/high-sucrose diet-induced weight gain compared to wildtype.Greater positive energy balance during HFHS feeding in male LPGC1a mice is associated with altered food intake patterns and reduced activity energy expenditure.Female LPGC1a mice do not have differences in short-term HFHS-induced body weight gain or energy metabolism compared to wildtype.Disruption of vagal signaling through common hepatic branch vagotomy increases short-term HFHS-induced weight gain in male wildtype mice, but does not alter male LPGC1a weight gain.

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