Obesity: Prevalence, Theories, Medical Consequences, Management, and Research Directions

Wilborn, Colin; Beckham, J; Campbell, B; Harvey, Travis; Galbreath, M; Bounty, Paul La; Nassar, E; Wismann, J; Kreider, Richard B.

doi:10.1186/1550-2783-2-2-4

Cited by 173 publications

(171 citation statements)

References 189 publications

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“…Previously, fats were supposed to play a leading role induce obesity because of including high-calorie, unlike this, some studies have been done about the carbohydrates induce obesity in recent years (1)(2)(3). According to Dr. Atkins trigger of obesity on foods are not fat and proteins, but carbohydrates.…”

Section: Introductionmentioning

confidence: 99%

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High Fatty Diet Effects on Rat Liver

et al. 2014

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Section: Introductionmentioning

confidence: 99%

“…According to Dr. Atkins trigger of obesity on foods are not fat and proteins, but carbohydrates. In Dr. Atkins diet method, daily carbohydrate intake is limited with maximum 20 grams protein and no restrictions are imposed on proteins and fats (1).…”

Section: Introductionmentioning

confidence: 99%

High Fatty Diet Effects on Rat Liver

et al. 2014

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“…It is known that obesity is related to impairments in lipid metabolism 26 . A research work by Coelho et al 27 in 153 medicine students (18 to 31 years old) revealed high levels of CT and TG only in obese individuals.…”

Section: Discussionmentioning

confidence: 99%

Efeito da dieta e do ciclismo indoor sobre a composição corporal e nível sérico lipídico

Valle¹,

Mello²,

Fortes³

et al. 2010

Arq. Bras. Cardiol.

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“…[49][50][51][52][53][54][55][56][57][58][59][60]. It is critical to understand that even with the most unfortunate genetic composition that predisposes an individual to metabolic disease [61], such as the well documented US Pima Indians with the world's highest prevalence of type 2 diabetes (38%), that physical activity (energy expenditure) and diet can have a profound effect on upon prevention.…”

Section: Animal Models With Dermis Issuesmentioning

confidence: 99%

Targeting energy expenditure via fuel switching and beyond

Geisler

2010

Diabetologia

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Since over-nutrition accelerates the development of obesity, progression to type 2 diabetes, and the associated co-morbidity and mortality, there has been a keen interest in therapeutic interventions targeting mechanisms that may curb appetite, increase energy expenditure or at least attenuate insulin resistance. Over the past decade, numerous peri-mitochondrial targets in the de novo lipid synthesis pathway have been linked to an increase in energy expenditure and the drug development industry has pursued the gene products involved as candidates to develop drugs against. The basis of this link, and specifically the premise that lowering tissue and cellular malonyl-CoA can increase energy expenditure, is scrutinised here. The argument presented is that fuel switching as effected by changes in cellular malonyl-CoA concentrations will not trigger the mitochondria to increase energy expenditure because: (1) an increase in beta-oxidation by lowering respiratory exchange ratio (indicative of the metabolic fuel consumed) does not equal an increase in energy expenditure (how rapidly fuel is consumed); (2) the ATP:oxygen ratios (i.e. ATP energy made:oxygen required for the reaction) are similar when metabolising lipids (2.8) vs glucose (3.0); (3) substrate availability (NEFA) does not drive energy expenditure in vivo; and (4) the availability of ADP in the mitochondrial matrix determines the rate of energy expenditure, not the availability of fuel to enter the mitochondrial matrix. To increase mitochondrial energy expenditure, work must be done (exercise) and/or the mitochondrial proton leak must be enhanced, both of which increase availability of ADP. In fact, despite the historic taboo of chemical uncoupling, this mechanism validated in humans is closest on task to increasing whole-body energy expenditure. Chemical uncoupling mimics the naturally occurring phenomenon of proton leak, accelerating the metabolism of glucose and lipids. However, it is completely non-genomic (i.e. the target is a location, not a gene product) and is not associated with addiction or mood alterations common to satiety agents. A significant hurdle for drug development is to discover a safe mitochondrial uncoupler and to formulate it potentially as a pro-drug and/or oral pump, to avoid the issue of overdosing experienced in the 1930s. The potential therapeutic impact of such a compound for an overnutritioned patient population could be profound. If effective, the mitochondrial uncoupler mechanism could resolve many of the associated diseases such as type 2 diabetes, hypertension, obesity, depression, sleep apnoea, non-alcoholic steatohepatitis, insulin resistance and hyperlipidaemia, therefore becoming a 'disease-modifying therapy'.

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Obesity: Prevalence, Theories, Medical Consequences, Management, and Research Directions

Cited by 173 publications

References 189 publications

High Fatty Diet Effects on Rat Liver

High Fatty Diet Effects on Rat Liver

Efeito da dieta e do ciclismo indoor sobre a composição corporal e nível sérico lipídico

Targeting energy expenditure via fuel switching and beyond

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