<i>In Vitro</i>lipolysis is associated with whole‐body lipid oxidation and weight gain in humans

Frankl, J; Piaggi, Paolo; Foley, James E.; Krakoff, Jonathan; Votruba, Susanne B.

doi:10.1002/oby.21670

Cited by 14 publications

(8 citation statements)

References 30 publications

(32 reference statements)

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“…In individuals who are metabolically inflexible to dietary fats, lipolysis may increase to a smaller degree during a high-fat diet (34). We have previously demonstrated that lower rates of in vitro lipolysis are associated with higher 24-h RQ and lower LIPOX during eucaloric feeding, and these individuals with reduced lipolysis gained more weight at follow-up as a result of an increase in FM (35). Supportive of a causal role for lipolysis in determining the degree of metabolic flexibility, we found that higher fasting concentrations of NEFA, a product of fat cell lipolysis (36), and regulators of LIPOX with the highest 24-h RQ during EBL and standard eucaloric feeding.…”

Section: Discussionmentioning

confidence: 97%

Impaired Metabolic Flexibility to High-Fat Overfeeding Predicts Future Weight Gain in Healthy Adults

et al. 2019

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The ability to switch fuels for oxidation in response to changes in macronutrient composition of diet (metabolic flexibility) may be informative of individuals’ susceptibility to weight gain. Seventy-nine healthy, weight-stable participants underwent 24-h assessments of energy expenditure and respiratory quotient (RQ) in a whole-room calorimeter during energy balance (EBL) (50% carbohydrate, 30% fat) and then during 24-h fasting and three 200% overfeeding diets in a crossover design. Metabolic flexibility was defined as the change in 24-h RQ from EBL during fasting and standard overfeeding (STOF) (50% carbohydrate, 30% fat), high-fat overfeeding (HFOF) (60% fat, 20% carbohydrate), and high-carbohydrate overfeeding (HCOF) (75% carbohydrate, 5% fat) diets. Free-living weight change was assessed after 6 and 12 months. Compared with EBL, RQ decreased on average by 9% during fasting and by 4% during HFOF but increased by 4% during STOF and by 8% during HCOF. A smaller decrease in RQ, reflecting a smaller increase in lipid oxidation rate, during HFOF but not during the other diets predicted greater weight gain at both 6 and 12 months. An impaired metabolic flexibility to acute HFOF can identify individuals prone to weight gain, indicating that an individual’s capacity to oxidize dietary fat is a metabolic determinant of weight change.

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Section: Discussionmentioning

confidence: 97%

Impaired Metabolic Flexibility to High-Fat Overfeeding Predicts Future Weight Gain in Healthy Adults

et al. 2019

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“…Mice with deficient lipolysis gain more weight in response to a high-fat diet, and in vitro adipocyte lipolytic activity has been found to be negatively associated with weight gain in humans. 61,62 Decreased lipolysis might reduce availability of substrates, possibly explaining the global reduction in lipid substances observed in patients at risk for weight gain. However, studies relating plasma lipidome to lipolytic rate and risk of weight gain are needed.…”

Section: Discussionmentioning

confidence: 99%

Metabolite and lipoprotein responses and prediction of weight gain during breast cancer treatment

et al. 2018

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BACKGROUND: Breast cancer treatment has metabolic side effects, potentially affecting risk of cardiovascular disease (CVD) and recurrence. We aimed to compare alterations in serum metabolites and lipoproteins during treatment between recipients and nonrecipients of chemotherapy, and describe metabolite profiles associated with treatment-related weight gain. METHODS: This pilot study includes 60 stage I/II breast cancer patients who underwent surgery and were treated according to national guidelines. Serum sampled pre-surgery and after 6 and 12 months was analysed by MR spectroscopy and mass spectrometry. In all, 170 metabolites and 105 lipoprotein subfractions were quantified. RESULTS: The metabolite and lipoprotein profiles of chemotherapy recipients and non-recipients changed significantly 6 months after surgery (p < 0.001). Kynurenine, the lipid signal at 1.55-1.60 ppm, ADMA, 2 phosphatidylcholines (PC aa C38:3, PC ae C42:1), alpha-aminoadipic acid, hexoses and sphingolipids were increased in chemotherapy recipients after 6 months. VLDL and small dense LDL increased after 6 months, while HDL decreased, with triglyceride enrichment in HDL and LDL. At baseline, weight gainers had less acylcarnitines, phosphatidylcholines, lyso-phosphatidylcholines and sphingolipids, and showed an inflammatory lipid profile. CONCLUSION: Chemotherapy recipients exhibit metabolic changes associated with inflammation, altered immune response and increased risk of CVD. Altered lipid metabolism may predispose for treatment-related weight gain.

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“…The 24‐h RQ has been shown to aggregate in family, and it has been suggested that it is at least in part genetically determined . The 24‐h RQ has also been shown to be statistically related to various individual characteristics such as percent body fat, plasma insulin, free fatty acid concentration, sex, ethnicity, age, waist circumference, fat mass and trunk fat mass, and adipocyte size and basal lipolysis measured in isolated hepatocytes from the periumbilical region . However, in perfect energy balance as well as in a given energy imbalance, the 24‐h RQ measured with a stable diet for some days only depends on the macronutrient composition of the diet and energy balance.…”

Section: Significance Of Rqmentioning

confidence: 99%

Low capacity to oxidize fat and body weight

Péronnet

Haman

2019

Obesity Reviews

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For a given positive energy balance, a low capacity to oxidize fat could contribute to weight gain (low fat oxidation hypothesis). This hypothesis is based on the arguments that for a given stable diet and food quotient (FQ), the respiratory quotient (RQ) is higher in obesity prone (OP) than in obesity resistant individuals (OR) and that a high RQ predicts higher future weight gain. A review of 42 studies shows that there is no convincing experimental support to these arguments and thus for the low fat oxidation hypothesis. A power analysis also shows that this hypothesis might be impossible to experimentally confirm because very large numbers of subjects would be needed to reject the null hypotheses that the 24-h RQ is not different in OP and OR or that future weight gain is not different in individuals with a low and high 24-h RQ at baseline. A re-examination of the significance of the 24-hour and fasting RQ also shows that the assumption underlying the low fat oxidation hypothesis that a high RQ reflects a low capacity to oxidize fat is not valid: For a stable diet, the 24-h RQ entirely depends on FQ and energy balance, and the fasting RQ mainly depends on the FQ and energy balance and on the size of glycogen stores. KEYWORDS food quotient, fuel partitioning, obesity, respiratory quotient 1 | INTRODUCTION It has been hypothesized that fat accumulation and weight gain could be favoured by two defects in fat oxidation: (a) a low intrinsic capacity to oxidize fat, 1-3 which characterizes "low fat oxidizers" 3,4 ("low fat oxidation hypothesis" of weight gain), or (b) a low ability to quickly adjust fat oxidation to an increase in fat intake, 5-8 which is one of the characteristics of individuals with "metabolic inflexibility" 9 ("metabolic inflexibility hypothesis" of weight gain). According to the low fat oxidation hypothesis of weight gain, for a given positive energy balance, fat oxidation is lower and fat accumulation is higher in individuals with a low than a high intrinsic capacity to oxidize fat, and over time, this could result in larger weight gains. 3 According to the "metabolic inflexibility hypothesis" of weight gain, for a given energy intake (EI), the slow adjustment of fat oxidation to an increase in fat intake in individuals with metabolic inflexibility favours fat storage with a compensatory increase in glucose oxidation from carbohydrate (CHO) stores. The result is a reduction in glycogen stores that could be a signal for increasing food intake and EI through the glycogenostatic model of the control of appetite. [5][6][7][8] Because of constant day-to-day variations in the percentage of fat in the diet, individuals with metabolic inflexibility could repeatedly accumulate small amounts of fat, which over time could lead to weight gain.List of abbreviations: ACC2, acetyl-CoA carboxylase 2; AICAR, 5-aminoimidazole-4-carboxamide ribonucleotide; AMPK, AMP-activated kinase; BMI, body mass index; CHO, carbohydrate; d, difference in 24-h RQ estimated between OP and OR; d/SD, standardized difference; EE, ...

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In Vitrolipolysis is associated with whole‐body lipid oxidation and weight gain in humans

Cited by 14 publications

References 30 publications

Impaired Metabolic Flexibility to High-Fat Overfeeding Predicts Future Weight Gain in Healthy Adults

Impaired Metabolic Flexibility to High-Fat Overfeeding Predicts Future Weight Gain in Healthy Adults

Metabolite and lipoprotein responses and prediction of weight gain during breast cancer treatment

Low capacity to oxidize fat and body weight

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