Adaptive thermogenesis in humans

Rosenbaum, Michael; Leibel, Rudolph L.

doi:10.1038/ijo.2010.184

Cited by 261 publications

(228 citation statements)

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“…As soon as energy expenditure is raised, and the balance becomes negative, the body may respond to that by increasing energy intake, and thus lead to weight regain [54 ]. The compensatory increase in energy intake has been demonstrated to be true, for example, in the described patients with high circulating levels of thyroid hormones.…”

Section: Measurements Of Skeletal Muscle Mitochondrial Uncoupling In mentioning

confidence: 89%

Skeletal muscle mitochondrial uncoupling, adaptive thermogenesis and energy expenditure

Berg

Lichtenbelt

Dijk

et al. 2011

Current Opinion in Clinical Nutrition and Metabolic Care

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IntroductionIn this review we set out to give an overview of the latest developments in the field of increasing whole-body energy expenditure via adaptive thermogenesis. In particular, we focus on the contribution of skeletal muscle mitochondrial uncoupling to whole-body energy expenditure and adaptive thermogenesis. In addition, we review the latest developments regarding the application of increasing adaptive thermogenesis to fight the obesity epidemic and the possibilities to achieve this goal by modulation of skeletal muscle mitochondrial uncoupling.In the modern Western society, the prevalence of obesity and obesity-related disorders are rising. The development of obesity is the result of a prolonged imbalance between energy intake and energy expenditure, and classically focus has been on reducing energy intake to correct this imbalance. However, although successful in the short term, the success rate of reducing energy intake in the long term is notoriously poor in humans, possibly due to the decrease in resting metabolic rate and exerciserelated energy expenditure as well as by promoting an unfavourable energy intake pattern [1 ,2 ,3 ]. The reduction in metabolic rate could be a risk factor for weight regain in itself, although the contribution of energy intake and expenditure to weight gain are still under debate [4 ]. Attempts to improve energy balance by exercise programmes have generated unclear results. Structured physical activity has been reported to increase total energy expenditure rates [5] but was found not to affect energy expenditure in another study [6]. Interestingly, Turner et al. [7 ] demonstrated that a 6-month progressive exercise programme does result in weight loss but the absolute reduction is less than expected due to an increase in energy intake. This stresses the importance to measure and report both sides of the energy balance. Thus, despite the obvious social and health benefits, the limited potency for physical exercise programmes to increase total energy expenditure may be due to the fact that the caloric cost per Purpose of review The prevalence of obesity is still increasing, despite obesity treatment strategies that aim at reducing energy intake. In addition to this, exercise programmes designed to increase energy expenditure have only a low efficiency and have generated mixed results. Therefore, strategies based on increasing energy expenditure via nonexercise means are currently under investigation. One novel strategy is the modulation of adaptive thermogenesis. Recent findings Among others, adaptive thermogenesis can be modulated by changing dietary composition, treatment with hormone mimetics as well as by cold exposure. In humans, a large part of the adaptive thermogenic response is, in addition to a putative role of brown adipose tissue, determined by the skeletal muscle mass via the process of mitochondrial uncoupling. Here, we describe the molecular processes involved in mitochondrial uncoupling, state-of-the-art techniques to measure mitochondrial uncoupling ...

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Section: Measurements Of Skeletal Muscle Mitochondrial Uncoupling In mentioning

confidence: 89%

Skeletal muscle mitochondrial uncoupling, adaptive thermogenesis and energy expenditure

Berg

Lichtenbelt

Dijk

et al. 2011

Current Opinion in Clinical Nutrition and Metabolic Care

View full text Add to dashboard Cite

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“…This model is an excellent one for the study of human obesity since, like most obese humans, it maintains its higher body weight and adipose set-points even when switched to a low-fat diet or after being calorically restricted for many weeks (291,302). This defense of a higher body weight set-point is what occurs in obese humans and is likely the reason for the high recidivism rate in the medical treatment of obesity and the extreme measures many previously obese individuals must undertake to keep off lost weight (326,448,538,557).…”

Section: Rat Modelsmentioning

confidence: 99%

Gene-Environment Interactions Controlling Energy and Glucose Homeostasis and the Developmental Origins of Obesity

Bouret

Levin

Ozanne

2015

Physiological Reviews

136

103

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LBouret S, Levin BE, Ozanne SE. Gene-Environment Interactions Controlling Energy and Glucose Homeostasis and the Developmental Origins of Obesity. Physiol Rev 95: 47-82, 2015; doi:10.1152/physrev.00007.2014.-Obesity and type 2 diabetes mellitus (T2DM) often occur together and affect a growing number of individuals in both the developed and developing worlds. Both are associated with a number of other serious illnesses that lead to increased rates of mortality. There is likely a polygenic mode of inheritance underlying both disorders, but it has become increasingly clear that the pre-and postnatal environments play critical roles in pushing predisposed individuals over the edge into a disease state. This review focuses on the many genetic and environmental variables that interact to cause predisposed individuals to become obese and diabetic. The brain and its interactions with the external and internal environment are a major focus given the prominent role these interactions play in the regulation of energy and glucose homeostasis in health and disease.

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“…11 This impressive recidivism rate after otherwise successful weight loss is partially due to poor adherence to lifestyle interventions and potently facilitated by coordinate actions of ancestral physiological responses designed to powerfully defend and restore body energy stores. 12 Indeed, weight loss initiated by reduced energy intake rapidly turns on a 'thrifty' program, which favors the eventual restoration of energy stores ( Figure 1, outer circle). 13 To this end, energy expenditure is suppressed in skeletal muscle, which is an important site of energy conservation during food restriction.…”

Section: Introductionmentioning

confidence: 99%

PGC-1α and exercise in the control of body weight

Summermatter

Handschin

2012

Int J Obes

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The increasing prevalence of obesity and its comorbidities represents a major threat to human health globally. Pharmacological treatments exist to achieve weight loss, but the subsequent weight maintenance is prone to fail in the long run. Accordingly, efficient new strategies to persistently control body weight need to be elaborated. Exercise and dietary interventions constitute classical approaches to reduce and maintain body weight, yet people suffering from metabolic diseases are often unwilling or unable to move adequately. The administration of drugs that partially mimic exercise adaptation might circumvent this problem by easing and supporting physical activity. The thermogenic peroxisome proliferator-activated receptor g coactivator 1a (PGC-1a) largely mediates the adaptive response of skeletal muscle to endurance exercise and is a potential target for such interventions. Here, we review the role of PGC-1a in mediating exercise adaptation, coordinating metabolic circuits and enhancing thermogenic capacity in skeletal muscle. We suggest a combination of elevated muscle PGC-1a and exercise as a modified approach for the efficient long-term control of body weight and the treatment of the metabolic syndrome.International Journal of Obesity (2012) 36, 1428 --1435; doi:10.1038/ijo.2012.12; published online 31 January 2012Keywords: PGC-1a; thermogenesis; energy expenditure; exercise; weight control INTRODUCTION Metabolic disorders are increasingly recognized as major threats to public health. Almost two-thirds of the adult Americans are already overweight (body mass index 425 kg m --2 ) and the prevalence will presumably rise in the future. 1 Projections indicate that 86.3% of the adult American population will be overweight and 51.1% will even have to be classified as obese (body mass index 430 kg m --2 ) by the year 2030. 2 Importantly, excessive body weight fosters the development of comorbidities such as hypertension, dyslipidemia, cancer, cardiovascular disease and diabetes. 3,4 A protracted energy imbalance where energy intake exceeds expenditure is considered as a key element in the etiology of metabolic impairments. 5,6 Reducing energy intake (by nutritional intervention), increasing energy expenditure (by physical activity) or the combination of both thus constitute cornerstones in the treatment of metabolic disorders. 7 Such lifestyle interventions generally lead to weight loss initially 7 and improve metabolic parameters, 8 but the majority of patients regain their weight in the long run. 9,10 A meta-analysis of studies published between 1931 and 1999 reveals a median success rate to maintain body weight after weight loss of a moderate 15%. 11 This impressive recidivism rate after otherwise successful weight loss is partially due to poor adherence to lifestyle interventions and potently facilitated by coordinate actions of ancestral physiological responses designed to powerfully defend and restore body energy stores. 12 Indeed, weight loss initiated by reduced energy intake rapidly turns on a 'thrift...

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Adaptive thermogenesis in humans

Cited by 261 publications

References 95 publications

Skeletal muscle mitochondrial uncoupling, adaptive thermogenesis and energy expenditure

Skeletal muscle mitochondrial uncoupling, adaptive thermogenesis and energy expenditure

Gene-Environment Interactions Controlling Energy and Glucose Homeostasis and the Developmental Origins of Obesity

PGC-1α and exercise in the control of body weight

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