Relationships of Serum Leptin to Body Composition and Resting Energy Expenditure

Campostano, A.; Grillo, Gustavo Fernandes; Bessarione, D.; Grandi, Roberta De; Adami, Gian Franco

doi:10.1055/s-2007-978951

Cited by 27 publications

(15 citation statements)

References 11 publications

(12 reference statements)

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“…In accordance with our results, in those studies in which RMR was adjusted for FFM and FM as outlined elsewhere (18) or in which the effects of FFM and FM were statistically eliminated by stepwise multiple regression analysis (5)(6)(7), no correlations between leptin and RMR were observed. The different statistical handling of the data may explain inconsistent results with regard to energy expenditure and leptin concentrations in adult humans.…”

Section: Discussionsupporting

confidence: 92%

“…Human studies in a variety of subjects investigating the relationship between serum leptin concentrations and energy expenditure are available with inconsistent results: some of these studies could not detect any association between leptin concentrations and resting metabolic rate (RMR) in adults with stable body weights and a wide range of body mass index (BMI) (5)(6)(7), and in patients with lung cancer cachexia (8); positive correlations were found in a group of 18 healthy men (9), in 25 free-living older African-American women (10), and in 18 elderly heart failure patients (11); a negative correlation was observed in a group of 45 obese subjects (12). Some of these inconsistencies may have methodological causes.…”

Section: Introductionmentioning

confidence: 99%

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Resting metabolic rate, body composition, and serum leptin concentrations in a free-living elderly population

Neuhäuser‐Berthold

Herbert

Luhrmann

et al. 2000

European Journal of Endocrinology

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Objective: The present study investigated the relationship between serum leptin concentrations and resting metabolic rate (RMR) in a large study group of elderly individuals with special consideration of body composition and body fat distribution as possible confounders. Design and methods: The subjects were 122 women (age: 69 Ϯ 6 years, body mass index (BMI): 26.3 Ϯ 3.6 kg/m 2 ) and 82 men (age: 69 Ϯ 5 years, BMI: 26.0 Ϯ 2.6 kg/m 2 ). RMR was measured by indirect calorimetry and body composition by the bioelectrical impedance method. Serum leptin levels were determined by radioimmunoassay.Results: There was a strong correlation between fat mass (FM) and serum leptin levels in both sexes. An age-related decline in leptin levels adjusted for FM was observed only in the women. After adjustment of RMR for both fat-free mass (FFM) and FM, leptin levels were not associated with RMR. In stepwise multiple regression analysis, FFM was the main predictor of RMR, explaining 35.8% and 47.6% of the variance of RMR in men and women respectively. FM did not explain variance in RMR in men, but accounted for 2.6% of the variance in RMR in women. Waist-hip-ratio and age influenced RMR only in males, explaining 5.7% and 4.0% of the variance in RMR respectively. Conclusion: Leptin is not a significant predictor of RMR in the elderly, but body composition and distribution of body fat are significantly associated with RMR.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Resting metabolic rate, body composition, and serum leptin concentrations in a free-living elderly population

Neuhäuser‐Berthold

Herbert

Luhrmann

et al. 2000

European Journal of Endocrinology

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“…Findings from some previous studies in humans have supported the hypothesis of a role of leptin in stimulating EE (7,(17)(18)(19)(20)(21), whereas others have failed to find such relationship (22)(23)(24)(25). Furthermore, inverse correlations between fasting plasma leptin and resting metabolic rate have been reported in obese subjects, in contrast to lean individuals, supporting the hypothesis of leptin-resistance in obesity (26 -28).…”

Section: Introductionmentioning

confidence: 87%

Leptin Levels Are Associated with Fat Oxidation and Dietary‐Induced Weight Loss in Obesity

et al. 2001

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Objective: To examine the relationship between fasting plasma leptin and 24-hour energy expenditure (EE), substrate oxidation, and spontaneous physical activity (SPA) in obese subjects before and after a major weight reduction compared with normal weight controls. To test fasting plasma leptin, substrate oxidations, and SPA as predictive markers of success during a standardized weight loss intervention. Research Methods and Procedures: Twenty-one nondiabetic obese (body mass index: 33.9 to 43.8 kg/m 2 ) and 13 lean (body mass index: 20.4 to 24.7 kg/m 2 ) men matched for age and height were included in the study. All obese subjects were reexamined after a mean weight loss of 19.2 kg (95% confidence interval: 15.1-23.4 kg) achieved by 16 weeks of dietary intervention followed by 8 weeks of weight stability. Twenty-four-hour EE and substrate oxidations were measured by whole-body indirect calorimetry. SPA was assessed by microwave radar. Results: In lean subjects, leptin adjusted for fat mass (FM) was correlated to 24-hour EE before (r ϭ Ϫ0.56, p Ͻ 0.05) but not after adjustment for fat free mass. In obese subjects, leptin correlated inversely with 24-hour and resting nonprotein respiratory quotient (r ϭ Ϫ0.47, p Ͻ 0.05 and r ϭ Ϫ0.50, p Ͻ 0.05) both before and after adjustments for energy balance. Baseline plasma leptin concentration, adjusted for differences in FM, was inversely related to the size of weight loss after 8 weeks (r ϭ Ϫ0.41, p ϭ 0.07), 16 weeks (r ϭ Ϫ0.51, p Ͻ 0.05), and 24 weeks (r ϭ Ϫ0.50, p Ͻ 0.05). Discussion: The present study suggests that leptin may have a stimulating effect on fat oxidation in obese subjects. A low leptin level for a given FM was associated with a greater weight loss, suggesting that obese subjects with greater leptin sensitivities are more successful in reducing weight.

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“…that the reporting system to the lipostatic control centre was underreporting their weight. However, apart from in a few unusual cases, leptin production in individuals with obesity is completely normal and they have very high levels of circulating leptin (Considine et al, 1996;Maffei et al, 1995;Adami et al, 1998;Campostano et al, 1998). Nevertheless, injecting leptin into mice reduced their body fatness Pellymounter et al, 1995, but see Mackintosh andHirsch 2001;Faouzi et al, 2007).…”

Section: Set-point Theorymentioning

confidence: 99%

The evolution of body fatness: trading off disease and predation risk

Speakman

2018

Journal of Experimental Biology

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Human obesity has a large genetic component, yet has many serious negative consequences. How this state of affairs has evolved has generated wide debate. The thrifty gene hypothesis was the first attempt to explain obesity as a consequence of adaptive responses to an ancient environment that in modern society become disadvantageous. The idea is that genes (or more precisely, alleles) predisposing to obesity may have been selected for by repeated exposure to famines. However, this idea has many flaws: for instance, selection of the supposed magnitude over the duration of human evolution would fix any thrifty alleles (famines kill the old and young, not the obese) and there is no evidence that hunter-gatherer populations become obese between famines. An alternative idea (called thrifty late) is that selection in famines has only happened since the agricultural revolution. However, this is inconsistent with the absence of strong signatures of selection at single nucleotide polymorphisms linked to obesity. In parallel to discussions about the origin of obesity, there has been much debate regarding the regulation of body weight. There are three basic models: the setpoint, settling point and dual-intervention point models. Selection might act against low and high levels of adiposity because food unpredictability and the risk of starvation selects against low adiposity whereas the risk of predation selects against high adiposity. Although evidence for the latter is quite strong, evidence for the former is relatively weak. The release from predation ∼2-million years ago is suggested to have led to the upper intervention point drifting in evolutionary time, leading to the modern distribution of obesity: the drifty gene hypothesis. Recent critiques of the dual-intervention point/ drifty gene idea are flawed and inconsistent with known aspects of energy balance physiology. Here, I present a new formulation of the dual-intervention point model. This model includes the novel suggestion that food unpredictability and starvation are insignificant factors driving fat storage, and that the main force driving up fat storage is the risk of disease and the need to survive periods of pathogen-induced anorexia. This model shows why two independent intervention points are more likely to evolve than a single set point. The molecular basis of the lower intervention point is likely based around the leptin pathway signalling. Determining the molecular basis of the upper intervention point is a crucial key target for future obesity research. A potential definitive test to separate the different models is also described.

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Relationships of Serum Leptin to Body Composition and Resting Energy Expenditure

Cited by 27 publications

References 11 publications

Resting metabolic rate, body composition, and serum leptin concentrations in a free-living elderly population

Resting metabolic rate, body composition, and serum leptin concentrations in a free-living elderly population

Leptin Levels Are Associated with Fat Oxidation and Dietary‐Induced Weight Loss in Obesity

The evolution of body fatness: trading off disease and predation risk

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