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      Diet, exercise or diet with exercise: comparing the effectiveness of treatment options for weight-loss and changes in fitness for adults (18–65 years old) who are overfat, or obese; systematic review and meta-analysis

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      Journal of Diabetes and Metabolic Disorders
      BioMed Central
      Obesity, Exercise, Comparison, Weight loss

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          Abstract

          There are number of means of methods to alter body composition, and metabolic issues, available for the adult who is overfat. The following is a systematic review and meta-analysis focused on comparing changes from treatment program for adults who are overfat based on analysis of aggregated effect size (ES) of inducing changes. So as to determine the relative effectiveness of such protocols and intervention plans of choice. This tiered meta-analysis of 66-population based studies, and 162-studywise groups, a clear pattern of ES being established across and within treatments. First, hypocaloric balance is necessary for changing body composition, but the effectiveness for establishing imbalance does not equate with the effectiveness for body compositional changes, or any biomarkers associated with metabolic issues. With analysis showing that there is a necessity to include exercise in combination with diet effectively elicit changes in body composition and biomarkers of metabolic issues. More importantly, the combination, resistance training (RT) was more effective than endurance training (ET) or combination of RT and ET, particularly when progressive training volume of 2-to-3 sets for 6-to-10 reps at an intensity of ≥75% 1RM, utilizing whole body and free-weight exercises, at altering body compositional measures (ES of 0.47, 0.30, and 0.40 for loss of BM, FM, and retention of FFM respectively) and reducing total cholesterol (ES = 0.85), triglycerides (ES = 0.86) and low-density lipoproteins (ES = 0.60). Additionally RT was more effective at reducing fasting insulin levels (ES = 3.5) than ET or ET and RT. Even though generally lower ES than RT, the inclusion of ET was more effective when performed at high intensity (e.g. ≥70% VO 2max or HR max for 30-minutes 3-4x’s/wk), or in an interval training style than when utilizing the relatively common prescribed method of low-to-moderate (e.g., 50-70% VO 2max or HR max for at least equal time) steady state method, ES of 0.35, 0.39, and 0.13 for BM, FM, and FFM respectively. Thus indicating that focus of treatment should be on producing a large metabolic stress (as induced by RT or high levels of ET) rather than an energetic imbalance for adults who are overfat.

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          Most cited references165

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          Muscles, exercise and obesity: skeletal muscle as a secretory organ.

          During the past decade, skeletal muscle has been identified as a secretory organ. Accordingly, we have suggested that cytokines and other peptides that are produced, expressed and released by muscle fibres and exert either autocrine, paracrine or endocrine effects should be classified as myokines. The finding that the muscle secretome consists of several hundred secreted peptides provides a conceptual basis and a whole new paradigm for understanding how muscles communicate with other organs, such as adipose tissue, liver, pancreas, bones and brain. However, some myokines exert their effects within the muscle itself. Thus, myostatin, LIF, IL-6 and IL-7 are involved in muscle hypertrophy and myogenesis, whereas BDNF and IL-6 are involved in AMPK-mediated fat oxidation. IL-6 also appears to have systemic effects on the liver, adipose tissue and the immune system, and mediates crosstalk between intestinal L cells and pancreatic islets. Other myokines include the osteogenic factors IGF-1 and FGF-2; FSTL-1, which improves the endothelial function of the vascular system; and the PGC-1α-dependent myokine irisin, which drives brown-fat-like development. Studies in the past few years suggest the existence of yet unidentified factors, secreted from muscle cells, which may influence cancer cell growth and pancreas function. Many proteins produced by skeletal muscle are dependent upon contraction; therefore, physical inactivity probably leads to an altered myokine response, which could provide a potential mechanism for the association between sedentary behaviour and many chronic diseases.
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            Adipose tissue, adipokines, and inflammation.

            White adipose tissue is no longer considered an inert tissue mainly devoted to energy storage but is emerging as an active participant in regulating physiologic and pathologic processes, including immunity and inflammation. Macrophages are components of adipose tissue and actively participate in its activities. Furthermore, cross-talk between lymphocytes and adipocytes can lead to immune regulation. Adipose tissue produces and releases a variety of proinflammatory and anti-inflammatory factors, including the adipokines leptin, adiponectin, resistin, and visfatin, as well as cytokines and chemokines, such as TNF-alpha, IL-6, monocyte chemoattractant protein 1, and others. Proinflammatory molecules produced by adipose tissue have been implicated as active participants in the development of insulin resistance and the increased risk of cardiovascular disease associated with obesity. In contrast, reduced leptin levels might predispose to increased susceptibility to infection caused by reduced T-cell responses in malnourished individuals. Altered adipokine levels have been observed in a variety of inflammatory conditions, although their pathogenic role has not been completely clarified.
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              Recent advances in the relationship between obesity, inflammation, and insulin resistance.

              It now appears that, in most obese patients, obesity is associated with a low-grade inflammation of white adipose tissue (WAT) resulting from chronic activation of the innate immune system and which can subsequently lead to insulin resistance, impaired glucose tolerance and even diabetes. WAT is the physiological site of energy storage as lipids. In addition, it has been more recently recognized as an active participant in numerous physiological and pathophysiological processes. In obesity, WAT is characterized by an increased production and secretion of a wide range of inflammatory molecules including TNF-alpha and interleukin-6 (IL-6), which may have local effects on WAT physiology but also systemic effects on other organs. Recent data indicate that obese WAT is infiltrated by macrophages, which may be a major source of locally-produced pro-inflammatory cytokines. Interestingly, weight loss is associated with a reduction in the macrophage infiltration of WAT and an improvement of the inflammatory profile of gene expression. Several factors derived not only from adipocytes but also from infiltrated macrophages probably contribute to the pathogenesis of insulin resistance. Most of them are overproduced during obesity, including leptin, TNF-alpha, IL-6 and resistin. Conversely, expression and plasma levels of adiponectin, an insulin-sensitising effector, are down-regulated during obesity. Leptin could modulate TNF-alpha production and macrophage activation. TNF-alpha is overproduced in adipose tissue of several rodent models of obesity and has an important role in the pathogenesis of insulin resistance in these species. However, its actual involvement in glucose metabolism disorders in humans remains controversial. IL-6 production by human adipose tissue increases during obesity. It may induce hepatic CRP synthesis and may promote the onset of cardiovascular complications. Both TNF-alpha and IL-6 can alter insulin sensitivity by triggering different key steps in the insulin signalling pathway. In rodents, resistin can induce insulin resistance, while its implication in the control of insulin sensitivity is still a matter of debate in humans. Adiponectin is highly expressed in WAT, and circulating adiponectin levels are decreased in subjects with obesity-related insulin resistance, type 2 diabetes and coronary heart disease. Adiponectin inhibits liver neoglucogenesis and promotes fatty acid oxidation in skeletal muscle. In addition, adiponectin counteracts the pro-inflammatory effects of TNF-alpha on the arterial wall and probably protects against the development of arteriosclerosis. In obesity, the pro-inflammatory effects of cytokines through intracellular signalling pathways involve the NF-kappaB and JNK systems. Genetic or pharmacological manipulations of these effectors of the inflammatory response have been shown to modulate insulin sensitivity in different animal models. In humans, it has been suggested that the improved glucose tolerance observed in the presence of thiazolidinediones or statins is likely related to their anti-inflammatory properties. Thus, it can be considered that obesity corresponds to a sub-clinical inflammatory condition that promotes the production of pro-inflammatory factors involved in the pathogenesis of insulin resistance.
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                Author and article information

                Contributors
                JClark@mcc.commnet.edu
                Journal
                J Diabetes Metab Disord
                J Diabetes Metab Disord
                Journal of Diabetes and Metabolic Disorders
                BioMed Central (London )
                2251-6581
                17 April 2015
                17 April 2015
                2015
                : 14
                : 31
                Affiliations
                Division of Mathematics, Science, and Health Careers; Department of Science, Manchester Community College, Manchester, CT 06045-1046 USA
                Article
                154
                10.1186/s40200-015-0154-1
                4429709
                25973403
                cd4aa3ad-2014-4d4d-bd69-635eade6ace6
                © Clark; licensee BioMed Central. 2015

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 12 March 2014
                : 2 April 2015
                Categories
                Review Article
                Custom metadata
                © The Author(s) 2015

                obesity,exercise,comparison,weight loss
                obesity, exercise, comparison, weight loss

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