Control of food intake by fatty acid oxidation

Scharrer, E.; Langhans, Wolfgang

doi:10.1152/ajpregu.1986.250.6.r1003

Cited by 113 publications

(116 citation statements)

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“…2DG administration increased food intake in OM rats on a high-fat diet. These results are similar to results from experiments with Sprague-Dawley rats (20,26). Carbohydrate and protein intakes were stimulated by MA in OM rats, but fat intake did not change.…”

Section: Discussionsupporting

confidence: 88%

“…This may be especially evident for S5B rats maintained on a high-fat diet. Alternatively, S5B rats may be more sensitive to the increase in circulating plasma fatty acids that are apparent after MA treatment (20,22), and this, in turn, antagonizes MA-induced feeding. Indeed, lipid infu-sion into the circulation can block the feeding response to MA (24).…”

Section: Discussionmentioning

confidence: 99%

“…Food intake can be stimulated by the administration of 2-deoxy-~-glucose (2DG) or P-mercaptoacetate (MA) (20,27). 2DG blocks glucose utilization by competitive an-tagonism of phosphohexose isomerase (28), and MA blocks fatty acid oxidation by competitive inhibition of mitochondrial acyl CoA dehydrogenases (2).…”

Section: Introductionmentioning

confidence: 99%

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Feeding Response to Mercaptoacetate in Osborne‐Mendel and S5B/PL Rats

1997

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SINGER, LORI K, DAVID A YORK, GEORGE A BRAY. Feeding response to mercaptoacetate in Osborne-Mendel and S5B/PL Rats. Obes. Res. 1997;5:587-594. The purpose of this experiment was to determine if Osborne-Mendel (OM) rats, which are susceptible to dietary-induced obesity, and SSB/PL (S5B) rats, which are resistant to dietary-induced obesity, differ in their feeding responses to mercaptoacetate (MA), which blocks fatty acid oxidation, or 2-deoxy-~-glucose (2DG), which blocks glucose utilization. 2DG (100 mgkg or 200 mg/ kg) increased food intake in both strains of rats on a high-fat diet (56% energy from fat). Mercaptoacetate (600 pmoVkg) increased food intake in OM but not S5B rats on a high-fat diet. When maintained on a low-fat diet (10% energy from fat), MA (400 pmoVkg or 600 pmoVkg) stimulated food intake in OM rats, whereas S5B rats increased food intake only after the highest dose of MA (600 prnolkg). MA stimulated carbohydrate and protein intake in OM rats maintained on a macronutrient selection diet, whereas S5B rats maintained on this diet did not significantly increase intake of any macronutrient after MA. These results demonstrate that OM and S5B rats have a similar food intake response to 2DG but a dissimilar response to MA. The variable response to MA in these strains may be due to a difference in peripheral or central signaling systems related to fatty acid oxidation or a difference in metabolic environments between the strains, which in turn affects the feeding response to MA. These studies suggest that a difference in control of fatty acid oxidation may account for the difference in susceptibility to obesity when eating a highfat diet.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

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Feeding Response to Mercaptoacetate in Osborne‐Mendel and S5B/PL Rats

1997

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“…of a high-GI diet led to decreased hepatic fat oxidation and then increased food consumption resulting in an increase in body weight and fat (17,18). Obesity has a strong correlation with the metabolic syndrome consisted of hypertension, dyslipidemia, insulin resistance, and type 2 diabetes.…”

Section: Articlesmentioning

confidence: 99%

“…This prolonged hyperinsulinemia would have the effect of directing nutrients from oxidation to storage (6). In fact, some studies demonstrated that hyperinsulinemia due to ingestion Articles Visuthranukul et alof a high-GI diet led to decreased hepatic fat oxidation and then increased food consumption resulting in an increase in body weight and fat (17,18). Obesity has a strong correlation with the metabolic syndrome consisted of hypertension, dyslipidemia, insulin resistance, and type 2 diabetes.…”

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confidence: 99%

Low-glycemic index diet may improve insulin sensitivity in obese children

et al. 2015

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ArticlesClinical Investigation nature publishing group BACKGROUND: A low-glycemic index (GI) diet may be beneficial for weight management due to its effect on insulin metabolism and satiety. METHODS: Obese children aged 9-16 y were randomly assigned either a low-GI diet or a low-fat diet (control group) for 6 mo. Body composition changes were measured by dualenergy X-ray absorptiometry and bioelectrical impedance analysis. Insulin sensitivity was measured by fasting plasma glucose and insulin. RESULTS: Fifty-two participants completed the study (mean age: 12.0 ± 2.0 y, 35 boys); both groups showed significantly decreased BMI z-score but similar changes in fat and fat-free mass. The low-GI group demonstrated a significant decline in fasting plasma insulin (22.2 ± 14.3 to 13.7 ± 10.9 mU/l; P = 0.004) and homeostatic model of assessment-insulin resistance (4.8 ± 3.3 to 2.9 ± 2.3; P = 0.007), whereas the control group did not. However, general linear model showed no significant difference in insulin resistance between groups after adjusting for baseline levels, suggesting that the greater reduction in insulin resistance in the low-GI group may be explained by higher baseline values. CONCLUSION: Despite subtle effects on body composition, a low-GI diet may improve insulin sensitivity in obese children with high baseline insulin. A bigger study in obese children with insulin resistance could be worthwhile to confirm our findings.C urrently, the prevalence of childhood obesity has been increasing worldwide (1). The Centers for Disease Control and Prevention reported that about 17% of children and adolescents in the United States aged 2-19 y were obese (2). Furthermore, the prevalence of the metabolic syndrome has been rapidly rising in obese children, and with it, the risk of cardiovascular disease (3). About 60% of overweight children have at least one cardiovascular disease risk factors such as hypertension, dyslipidemia, and insulin resistance. In addition, more than 25% of them have more than one type of cardiovascular disease risk factors (1). The common complications of childhood obesity are the metabolic syndrome (hypertension, dyslipidemia, insulin resistance, and type 2 diabetes), obstructive sleep apnea, nonalcoholic steatohepatitis, polycystic ovary syndrome, orthopedic complications, and premature atherosclerosis (4).At present, we are unable to describe the exact etiology of obesity, but one of the most common causes is an imbalance between energy intake and physical activity. Treatment of obesity is difficult and can be done by several approaches, including dietary control (such as low-fat, low-energy diet), physical activity program, behavioral modification (such as generating weight reduction goal, self-monitoring, as well as positive reinforcement by parents), and medical treatment. There are many pediatric patients seeking hospital-based obesity treatment. Most of them have one or more of the complications of obesity mentioned above as well as a loss of their self-esteem and social lives. In general, ...

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