scholarly journals Physical Exercise, Energy Expenditure and Weight Loss: An Assumption not Always Observed in Practice

Author(s):  
Vitor Barreto Paravidino ◽  
Mauro Felippe Felix Mediano ◽  
Rosely Sichieri

2019 ◽  
Vol 10 (1) ◽  
pp. 31-58
Author(s):  
Katarina Tomljenović Borer

The rapid global rise of obesity incurs a heavy personal and healthcare burden due to obesity-associated morbidities and shortening of life. The purpose of this review is to provide evidence-based strategies for prevention, reversal, and mitigation of obesity and its sequelae. To that end, this review highlights the features of human physiology that favor fat accretion and interfere with fat loss. Strategies for prevention of obesity include understanding the basis for the strong motivating properties of palatable food, for human inability to consciously detect calories eaten or calories expended through exercise, for metabolic and hormonal adaptations to negative energy balance that drive weight regain, and for evolutionary natural selection which likely led to high human capacity for fat storage. Reversal of obesity is difficult primarily due to metabolic, hormonal, and behavioral reactions to body fat loss. Reduced resting metabolic rate presents a physiological challenge whether the weight loss is achieved through dietary restriction or energy expenditure of exercise. Increased insulin sensitivity after body fat loss drives resynthesis of storage substrates including triglycerides in the adipose tissue, muscle glycogen, and proteins, thus contributing to weight regain. Reduced basal plasma leptin concentration elicits a strong hunger drive. Mitigation of obesity-associated morbidities involves adding exercise energy expenditure to deliberate control of the quantity of food eaten, reducing postprandial hyperinsulinemia by lowering the carbohydrate load of the diet, and exercising after, rather than before, the meals to facilitate improved glucose tolerance.



2009 ◽  
Vol 69 (1) ◽  
pp. 34-38 ◽  
Author(s):  
C. R. Hankey

Treatments to induce weight loss for the obese patient centre on the achievement of negative energy balance. This objective can theoretically be attained by interventions designed to achieve a reduction in energy intake and/or an increase in energy expenditure. Such ‘lifestyle interventions’ usually comprise one or more of the following strategies: dietary modification; behaviour change; increases in physical activity. These interventions are advocated as first treatment steps in algorithms recommended by current clinical obesity guidelines. Medication and surgical treatments are potentially available to those unable to implement ‘lifestyle interventions’ effectively by achieving losses of between 5 kg and 10 kg. It is accepted that the minimum of 5% weight loss is required to achieve clinically-meaningful benefits. Dietary treatments differ widely. Successful weight loss is most often associated with quantification of energy intake rather than macronutrient composition. Most dietary intervention studies secure a weight loss of between 5 kg and 10 kg after intervention for 6 months, with gradual weight regain at 1 year where weight changes are 3–4 kg below the starting weight. Some dietary interventions when evaluated at 2 and 4 years post intervention report the effects of weight maintenance rather than weight loss. Specific anti-obesity medications are effective adjuncts to weight loss, in most cases doubling the weight loss of those given dietary advice only. Greater physical activity alone increases energy expenditure by insufficient amounts to facilitate clinically-important weight losses, but is useful for weight maintenance. Weight losses of between half and three-quarters of excess body weight are seen at 10 years post intervention with bariatric surgery, making this arguably the most effective weight-loss treatment.



2018 ◽  
Vol 315 (4) ◽  
pp. R595-R608 ◽  
Author(s):  
Jacob D. Brown ◽  
Danielle McAnally ◽  
Jennifer E. Ayala ◽  
Melissa A. Burmeister ◽  
Camilo Morfa ◽  
...  

Long-acting glucagon-like peptide-1 (GLP-1) receptor (GLP-1R) agonists (GLP-1RA), such as exendin-4 (Ex4), promote weight loss. On the basis of a newly discovered interaction between GLP-1 and oleoylethanolamide (OEA), we tested whether OEA enhances GLP-1RA-mediated anorectic signaling and weight loss. We analyzed the effect of GLP-1+OEA and Ex4+OEA on canonical GLP-1R signaling and other proteins/pathways that contribute to the hypophagic action of GLP-1RA (AMPK, Akt, mTOR, and glycolysis). We demonstrate that OEA enhances canonical GLP-1R signaling when combined with GLP-1 but not with Ex4. GLP-1 and Ex4 promote phosphorylation of mTOR pathway components, but OEA does not enhance this effect. OEA synergistically enhanced GLP-1- and Ex4-stimulated glycolysis but did not augment the hypophagic action of GLP-1 or Ex4 in lean or diet-induced obese (DIO) mice. However, the combination of Ex4+OEA promoted greater weight loss in DIO mice than Ex4 or OEA alone during a 7-day treatment. This was due in part to transient hypophagia and increased energy expenditure, phenotypes also observed in Ex4-treated DIO mice. Thus, OEA augments specific GLP-1RA-stimulated signaling but appears to work in parallel with Ex4 to promote weight loss in DIO mice. Elucidating cooperative mechanisms underlying Ex4+OEA-mediated weight loss could, therefore, be leveraged toward more effective obesity therapies.



2017 ◽  
Vol 313 (6) ◽  
pp. E731-E736 ◽  
Author(s):  
Wenjuan Wang ◽  
Xiangzhi Meng ◽  
Chun Yang ◽  
Dongliang Fang ◽  
Xuemeng Wang ◽  
...  

Loss of body weight and fat mass is one of the nonmotor symptoms of Parkinson’s disease (PD). Weight loss is due primarily to reduced energy intake and increased energy expenditure. Whereas inadequate energy intake in PD patients is caused mainly by appetite loss and impaired gastrointestinal absorption, the underlying mechanisms for increased energy expenditure remain largely unknown. Brown adipose tissue (BAT), a key thermogenic tissue in humans and other mammals, plays an important role in thermoregulation and energy metabolism; however, it has not been tested whether BAT is involved in the negative energy balance in PD. Here, using the 6-hydroxydopamine (6-OHDA) rat model of PD, we found that the activity of sympathetic nerve (SN), the expression of Ucp1 in BAT, and thermogenesis were increased in PD rats. BAT sympathetic denervation blocked sympathetic activity and decreased UCP1 expression in BAT and attenuated the loss of body weight in PD rats. Interestingly, sympathetic denervation of BAT was associated with decreased sympathetic tone and lipolysis in retroperitoneal and epididymal white adipose tissue. Our data suggeste that BAT-mediated thermogenesis may contribute to weight loss in PD.





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