Obesity management – new perspectives

Obesity represents a growing threat for the health of population worldwide. The decline of physical activity and the passive overconsumption of energy-dense, high-fat diets are important factors that explain the increased prevalence of obesity. Despite many efforts, the prevention and the treatment of obesity are often a failure. Since obesity development is due to a chronic imbalance between energy intake and energy expenditure, the most important advice for the prevention and the treatment of this nutritional disorder remains the reduction of high-fat foods and the stimulation of fat oxidation by promoting physical activity. The recent advances in our understanding of the control of food intake and of energy expenditure offer the hope that new therapeutic agents will become available over the next decade. This article briefly presents our present understanding of the main mechanisms which are responsible for the increased prevalence of obesity and some new areas of research which may be promising for the prevention and treatment of this disease.

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The role of high-fat diets and physical activity in the regulation of body weight

British Journal Of Nutrition ◽

10.1017/s0007114500001720 ◽

2000 ◽

Vol 84 (4) ◽

pp. 417-427 ◽

Cited By ~ 161

Author(s):

Patrick Schrauwen ◽

Klaas R. Westerterp

Keyword(s):

Physical Activity ◽

Dietary Fat ◽

High Fat Diet ◽

Fat Oxidation ◽

Fat Intake ◽

High Fat ◽

High Fat Diets ◽

Prevalence Of Obesity ◽

Fat Diets

The prevalence of obesity is increasing in westernized societies. In the USA the age-adjusted prevalence of BMI ≫30 kg/m2 increased between 1960 and 1994 from 13 % to 23 % for people over 20 years of age. This increase in the prevalence of obesity has been attributed to an increased fat intake and a decreased physical activity. However, the role of the impact of the level of dietary fat intake on human obesity has been challenged. High-fat diets, due to their high energy density, stimulate voluntary energy intake. An increased fat intake does not stimulate its own oxidation but the fat is stored in the human body. When diet composition is isoenergetically switched from low to high fat, fat oxidation only slowly increases, resulting in positive fat balances on the short term. Together with a diminished fat oxidation capacity in pre-obese subjects, high-fat diets can therefore be considered to be fattening. Another environmental factor which could explain the increasing prevalence of obesity is a decrease in physical activity. The percentage of body fat is negatively associated with physical activity and exercise has pronounced effects on energy expenditure and substrate oxidation. High-intensity exercise, due to a lowering of glycogen stores, can lead to a rapid increase in fat oxidation, which could compensate for the consumption of high-fat diets in westernized societies. Although the consumption of high-fat diets and low physical activity will easily lead to the development of obesity, there is still considerable inter-individual variability in body composition in individuals on similar diets. This can be attributed to the genetic background, and some candidate genes have been discovered recently. Both leptin and uncoupling protein have been suggested to play a role in the prevention of diet-induced obesity. Indeed, leptin levels are increased on a high-fat diet but this effect can be attributed to the increased fat mass observed on the high-fat diet. No effect of a high-fat diet per se on leptin levels is observed. Uncoupling proteins are increased by high-fat diets in rats but no data are available in human subjects yet. In conclusion, the increased intake of dietary fat and a decreasing physical activity level are the most important environmental factors explaining the increased prevalence of obesity in westernized societies.

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Interactions between physical activity and diet in the regulation of body weight

Proceedings of The Nutrition Society ◽

10.1017/s0029665100000215 ◽

2000 ◽

Vol 59 (2) ◽

pp. 193-198 ◽

Cited By ~ 27

Author(s):

Melanie S. Moore

Keyword(s):

Physical Activity ◽

Energy Expenditure ◽

Energy Intake ◽

Epidemiological Data ◽

Positive Energy ◽

Short Term ◽

High Fat Diets ◽

Prevalence Of Obesity ◽

Positive Energy Balance ◽

Fat Diets

The increasing worldwide prevalence of obesity suggests that there is a chronic positive energy balance. This situation implies poor coupling between energy intake and energy expenditure, but the contribution of each of these factors remains unclear. Epidemiological data suggests that physical activity has a role in the prevention of weight gain, although there is little evidence that it has a beneficial role in weight loss. High-fat diets have also been implicated, evidence from a variety of sources suggests that diets high in fat undermine appetite regulatory mechanisms. There has been much research to investigate the coupling between energy expenditure and energy intake in the short term in an attempt to elucidate some of the mechanisms involved. However, mechanisms regulating appetite are very complex, and it is currently unclear at which points physical activity and diet may have an influence.

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High fat diets are associated with higher abdominal adiposity regardless of physical activity in adolescents; the HELENA study

Clinical Nutrition ◽

10.1016/j.clnu.2013.10.008 ◽

2014 ◽

Vol 33 (5) ◽

pp. 859-866 ◽

Cited By ~ 15

Author(s):

Idoia Labayen ◽

Jonatan R. Ruiz ◽

Francisco B. Ortega ◽

Inge Huybrechts ◽

Gerardo Rodríguez ◽

...

Keyword(s):

Physical Activity ◽

Abdominal Adiposity ◽

High Fat ◽

High Fat Diets ◽

Fat Diets ◽

Helena Study

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Dietary carbohydrates modulate metabolic and β-cell adaptation to high-fat diet-induced obesity

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00539.2019 ◽

2020 ◽

Vol 318 (6) ◽

pp. E856-E865 ◽

Cited By ~ 2

Author(s):

Tracy K. Her ◽

William S. Lagakos ◽

Matthew R. Brown ◽

Nathan K. LeBrasseur ◽

Kuntol Rakshit ◽

...

Keyword(s):

Energy Expenditure ◽

Cell Biology ◽

Dietary Carbohydrates ◽

High Fat ◽

Severe Restriction ◽

Β Cell ◽

Pancreatic Islet Cell ◽

Ketogenic Diets ◽

High Fat Diets ◽

Fat Diets

Obesity is associated with several chronic comorbidities, one of which is type 2 diabetes mellitus (T2DM). The pathogenesis of obesity and T2DM is influenced by alterations in diet macronutrient composition, which regulate energy expenditure, metabolic function, glucose homeostasis, and pancreatic islet cell biology. Recent studies suggest that increased intake of dietary carbohydrates plays a previously underappreciated role in the promotion of obesity and consequent metabolic dysfunction. Thus, in this study, we utilized mouse models to test the hypothesis that dietary carbohydrates modulate energetic, metabolic, and islet adaptions to high-fat diets. To address this, we exposed C57BL/6J mice to 12 wk of 3 eucaloric high-fat diets (>60% calories from fat) with varying total carbohydrate (1–20%) and sucrose (0–20%) content. Our results show that severe restriction of dietary carbohydrates characteristic of ketogenic diets reduces body fat accumulation, enhances energy expenditure, and reduces prevailing glycemia and insulin resistance compared with carbohydrate-rich, high-fat diets. Moreover, severe restriction of dietary carbohydrates also results in functional, morphological, and molecular changes in pancreatic islets highlighted by restricted capacity for β-cell mass expansion and alterations in insulin secretory response. These studies support the hypothesis that low-carbohydrate/high-fat diets provide antiobesogenic benefits and suggest further evaluation of the effects of these diets on β-cell biology in humans.

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Selective Inactivation of Socs3 in SF1 Neurons Improves Glucose Homeostasis without Affecting Body Weight

Endocrinology ◽

10.1210/en.2008-0805 ◽

2008 ◽

Vol 149 (11) ◽

pp. 5654-5661 ◽

Cited By ~ 59

Author(s):

Ren Zhang ◽

Harveen Dhillon ◽

Huali Yin ◽

Akihiko Yoshimura ◽

Bradford B. Lowell ◽

...

Keyword(s):

Body Weight ◽

Food Intake ◽

Energy Expenditure ◽

Glucose Homeostasis ◽

Leptin Resistance ◽

High Fat ◽

Leptin Signaling ◽

Leptin Sensitivity ◽

High Fat Diets ◽

Fat Diets

Suppressor of cytokine signaling 3 (Socs3) has been identified as a mediator of central leptin resistance, but the identity of specific neurons in which Socs3 acts to suppress leptin signaling remains elusive. The ventromedial hypothalamus (VMH) was recently shown to be an important site for leptin action because deleting leptin receptor within VMH neurons causes obesity. To examine the role of VMH Socs3 in leptin resistance and energy homeostasis, we generated mice lacking Socs3 specifically in neurons positive for steroidogenic factor 1 (SF1), which is expressed abundantly in the VMH. These mice had increased phosphorylation of signal transducer and activator of transcription-3 in VMH neurons, suggesting improved leptin signaling, and consistently, food intake and weight-reducing effects of exogenous leptin were enhanced. Furthermore, on either chow or high-fat diets, these mice had reduced food intake. Unexpectedly, energy expenditure was reduced as well. Mice lacking Socs3 in SF1 neurons, despite no change in body weight, had improved glucose homeostasis and were partially protected from hyperglycemia and hyperinsulinemia induced by high-fat diets. These results suggest that Socs3 in SF1 neurons negatively regulates leptin signaling and plays important roles in mediating leptin sensitivity, glucose homeostasis, and energy expenditure.

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Non-Fasting Factor VII Coagulant Activity (FVII:C) Increased by High-Fat Diet

Thrombosis and Haemostasis ◽

10.1055/s-0038-1642518 ◽

1994 ◽

Vol 71 (06) ◽

pp. 755-758 ◽

Cited By ~ 46

Author(s):

E M Bladbjerg ◽

P Marckmann ◽

B Sandström ◽

J Jespersen

Keyword(s):

High Fat Diet ◽

Fat Content ◽

Factor Vii ◽

Amidolytic Activity ◽

High Fat ◽

Low Fat Diet ◽

Increased Risk ◽

Coagulant Activity ◽

High Fat Diets ◽

Fat Diets

SummaryPreliminary observations have suggested that non-fasting factor VII coagulant activity (FVII:C) may be related to the dietary fat content. To confirm this, we performed a randomised cross-over study. Seventeen young volunteers were served 2 controlled isoenergetic diets differing in fat content (20% or 50% of energy). The 2 diets were served on 2 consecutive days. Blood samples were collected at 8.00 h, 16.30 h and 19.30 h, and analysed for triglycerides, FVII coagulant activity using human (FVII:C) or bovine thromboplastin (FVII:Bt), and FVII amidolytic activity (FVIPAm). The ratio FVII:Bt/FVII:Am (a measure of FVII activation) increased from fasting levels on both diets, but most markedly on the high-fat diet. In contrast, FVII: Am (a measure of FVII protein) tended to decrease from fasting levels on both diets. FVII:C rose from fasting levels on the high-fat diet, but not on the low-fat diet. The findings suggest that high-fat diets increase non-fasting FVII:C, and consequently may be associated with increased risk of thrombosis.

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