Physical training in human obesity. 3. Effects of long-term physical training on body composition

Eight severely obese patients with adipose tissue hypercellularity, elevated body cell mass, and a juvenile onset of obesity were subjected to physical training during 6 mo without dietary restrictions. The training program was of 35-min duration three times weekly and followed a fixed schedule individualized to the working ability of each subject, so that the heart rate was 10–15 beats below maximal during three 5-min periods of each training session. Body weight, body cell mass, and body fat showed no significant changes after 3 or 6 mo of training. Fasting plasma insulin decreased after 3 mo of training, but fasting blood glucose was not changed. After 6 mo plasma insulin values were still decreased. Now glucose tolerance had also improved, and plasma triglycerides showed a trend to lower values. The results suggest that the lack of body fat decrease after the long training period might be characteristic for subjects with the type of severe obesity studied, because in a previous study¹ a similar, although lighter, training procedure produced a marked body fat decrease in patients without severe obesity.     

Angiogenesis in adipose tissue and obesity

Angiogenesis - While most tissues exhibit their greatest growth during development, adipose tissue is capable of additional massive expansion in adults. Adipose tissue expandability is advantageous...     

Effects of submaximal physical exercise on adipose tissue metabolism in man

In order to follow early metabolic adaptations in adipose tissue, which may lead to a decrease in fat cell size and body fat obtained by physical training, two sets of experiments were performed. Obese subjects and a control group exercised on a bicycle at two-thirds of maximal working capacity for one hour. Twenty-four hours thereafter, either on ad libitum diet, or on an isocaloric diet supplemented with calories corresponding to the expanded calories during the work load, an adipose tissue biopsy was taken and fat cell metabolism studied. In obese subjects on and ad libitum or on an isocaloric diet the lipolytic process was increased after the exercise but no significant effects were found on the rates of glucose metabolism. Furthermore, a relationship between cell surface and metabolism was found before, but not after, the work in all groups. No changes were seen in lipoprotein lipase activity. Obese subjects on a controlled diet showed a somewhat higher insulin and catecholamine responsiveness of adipocytes than was the case in the obese subjects on an ad libitum diet. This may well be due to the differences in carbohydrate intake, a factor of importance for hormonal responsiveness of fat cells. The increased basal lipolysis after exercise may be caused by the release of lipolytic hormones, and may well be the first sign of an adaption of the organism to diminish the fat stores as seen in physically trained subjects.     

Perilipin expression in human adipose tissue is elevated with obesity

The perilipins are highly phosphorylated adipocyte proteins that are localized at the surface of the lipid droplet. With activation by protein kinase A, perilipins translocate away from the lipid droplet and allow hormone-sensitive lipase to hydrolyze the adipocyte triglycerides to release nonesterified fatty acids (NEFA). Because of the potential importance of adipocyte lipolysis to obesity and insulin resistance, we measured perilipin protein and mRNA levels in nondiabetic subjects with varying degrees of insulin resistance. By Northern and Western blotting, we could detect perilipin A, but not perilipin B. Perilipin A protein and mRNA levels were quantitated and were highly correlated with each other. There was a significant positive relationship between perilipin expression and obesity (r = 0.55; P < 0.01, perilipin mRNA vs. percent body fat). However, there was no significant relationship between perilipin expression and blood NEFA, nor was there a significant relationship between perilipin expression and insulin resistance, using the insulin sensitivity index derived from the iv glucose tolerance test with minimal modeling. In addition, there was no significant relationship between perilipin and adipocyte or systemic inflammatory markers, such as TNFalpha, IL-6, and adiponectin. Thus, perilipin was elevated in obese subjects, perhaps as a compensatory mechanism to limit basal lipolysis. However, there was no relationship between perilipin and insulin resistance.     

Peculiar distribution of adipose tissue in patients with congenital generalized lipodystrophy.

Congenital generalized lipodystrophy (CGL) is a rare genetic disease with extreme paucity of fat from birth which is believed to be generalized, involving the whole body. Affected patients are characterized by severe insulin resistance. Sites of adipose tissue distribution in patients with CGL have not been studied systematically. Therefore, the fat distribution in three women (17-20 yr old) with CGL was investigated. Determination of body composition by underwater volume displacement suggested the complete absence of body fat (range, -3 to -7%; normal, 15-25%). Whole body magnetic resonance imaging, however, detected fat in particular anatomical sites, namely in orbits, palms and soles, and periarticular and epidural regions. Some fat was also localized in the tongue, breasts, vulva, and buccal area. Fat in other subcutaneous areas, intraabdominal and intrathoracic regions, and bone marrow was essentially absent. Thus, patients with CGL do not have a complete absence of body fat; of interest, fat is present in those sites where adipose tissue may be serving mainly a mechanical function. Patients with CGL, therefore, provided a unique opportunity to identify the various sites of localization of "mechanical" adipose tissue in the human body. Our study suggests that the genetic defect in CGL results in poor growth and development of metabolically active adipose tissue, whereas mechanical adipose tissue is well preserved.     

The role of brown adipose tissue in human obesity

It is widely accepted that newborn humans are provided with brown adipose tissue (BAT) and that adult humans lack, or have only a small amount, of it. Therefore the physiological role of BAT in humans is debated. It is quite clear that BAT in rodents has an important role in the prevention and therapy of obesity and diabetes and specific drugs can induce BAT development in adult animals. New concepts regarding the biology of adipose tissues in mammals have been developed during the last years leading to the hope for the development of BAT in human adults as a new challenge for the treatment of obesity and related diseases. These new concepts are basic to understanding the above-proposed therapeutic strategy and are the concept of the adipose organ and the concept of transdifferentiation. In this paper these new concepts will be explained together with a review of available scientific data on human BAT.     

Effects of physical training on anthropometrics,physical and physiological capacities in individuals with obesity: A systematic review

Increasing the amount of physical activity is an important strategy for weight loss. This systematic review summarizes recent findings on the effects of physical training on anthropometric characteristics, physical performances and physiological capacities in individuals with overweight and obesity. A systematic literature search strategy was conducted from inception until June 2019 using four electronic databases that identified 2,708 records. After screening for titles, abstracts and full texts, 116 studies were included in our final analysis. Both aerobic (e.g., endurance training) and anaerobic training (e.g., high‐intensity training, resistance training) improved body composition and physical fitness indicators in adults, adolescents and children with obesity (effect size: 0.08 < d < 2.67, trivial to very large). This systematic review suggests that both low‐ and high‐intensity training significantly reduced body weight and fat mass while increasing fat‐free mass in individuals with obesity (effect size: 0.04 <d <3.2, trivial to very large). A significant increase in VO_2max also occurs in individuals with obesity in response to aerobic training or high‐intensity interval training (effect size: 0.13 < d < 6.24, trivial to very large). Further studies are needed to define the optimal combination of training intensity and duration needed to produce the most efficacious results in individuals with obesity.     

Effects of physical training on beta-adrenergic receptors in rat myocardial tissue

A diminished sympathetic activity has been related to training bradycardia seen at rest and during exercise. In order to evaluate if changes in heart adrenergic receptors can be one of the mechanisms by which the sympathetic responsiveness could be decreased by physical training, the number and affinity of beta-adrenergic receptors were determined in heart ventricular tissue of rats submitted to a 10-week running programme. Binding studies were done at different concentrations of (-)[3H] dihydroalprenolol (DHA) (0.5 to 14.4 nmol X litre-1) with ventricular membrane preparations from control and trained rats. Direct linear plot analysis revealed that physical training reduced the total number (1933 +/- 192 vs 2922 +/- 211 fmol X ventricles-1; P less than 0.01) density of beta-adrenergic receptors expressed either as fmol X mg-1 of membrane protein (34 +/- 3 vs 43 +/- 3; P less than 0.05) or as fmol X g-1 ventricle (1740 +/- 170 vs 2308 +/- 155; P less than 0.05). There was no significant change in the dissociation constant (3.11 +/- 0.14 vs 4.08 +/- 0.51 nmol X litre-1; P greater than 0.05). Basal plasma noradrenaline levels were not affected by training (116 +/- 18 vs 101 +/- 14 pg X cm-3; P greater than 0.10); however the adrenaline values were significantly higher in trained rats (91 +/- 16 vs 47 +/- 7 pg X cm-3; P less than 0.05). These data indicate that physical training induces changes at the level of beta-adrenergic receptors and this may partly explain the bradycardia seen in trained subjects and animals.     

Brown adipose tissue as an anti‐obesity tissue in humans

During the 11th Stock Conference held in Montreal, Quebec, Canada, world‐leading experts came together to present and discuss recent developments made in the field of brown adipose tissue biology. Owing to the vast capacity of brown adipose tissue for burning food energy in the process of thermogenesis, and due to demonstrations of its presence in adult humans, there is tremendous interest in targeting brown adipose tissue as an anti‐obesity tissue in humans. However, the future of such therapeutic approaches relies on our understanding of the origin, development, recruitment, activation and regulation of brown adipose tissue in humans. As reviewed here, the 11th Stock Conference was organized around these themes to discuss the recent progress made in each aspect, to identify gaps in our current understanding and to further provide a common groundwork that could support collaborative efforts aimed at a future therapy for obesity, based on brown adipose tissue thermogenesis.     

Effects of long-term physical training on body fat, metabolism, and blood pressure in obesity.

Twenty-seven women with varying degrees of obesity were physically trained for 6 mo on an ad lib. diet. Body fat changes were positively correlated with the number of fat cells in adipose tissue. Obese women with fewer fat cells decreased in weight during training whereas women with severe obesity and an increased number of fat cells even gained weight. Blood pressure decreased consistently after training. Blood pressure elevation was not associated with body fat mass, nor was a decrease in blood pressure associated with a decrease in body fat or with pretraining blood pressure level. There were, instead, correlations between decreases in blood pressure on the one hand and initial concentrations and decreases in plasma insulin and triglycerides and blood glucose on the other. These results suggest an association between elevated blood pressure and metabolic variables. The possibility of treating and preventing early essential hypertension with methods that also correct the metabolic derangement, such as diet and exercise, should be given high priority in further research.     

Acylation-stimulating protein precursor proteins in adipose tissue in human obesity

Recent reports have suggested a link between acylation-stimulating protein (ASP) and complement C3 with obesity, insulin resistance, coronary artery disease, and hyperlipidemia. Our aim was to examine the mRNA expression of C3 and other factors related to ASP production (such as factor B and adipsin) in adipose tissue. The influence of gender and obesity was examined in subcutaneous (SC) and omental (OM) tissues from 16 males and 16 females with body mass index (BMI) from 20 to 54 kg/m². The results demonstrate that factor B mRNA expression is higher in males than females in both SC and OM tissues. In female SC tissue, C3 and adipsin mRNA decrease with increasing BMI (r = 0.557, P = .025 and r = 0.717 P = .002, respectively), with no change in factor B. By contrast, in males there was a pronounced increase in C3, adipsin, and factor B in OM tissue with increasing BMI (r = 0.759 P = .001, r = 0.650 P = .006, and r = 0.568 P = .022, respectively). Of note, however, in both men and women there was a marked increase in the OM/SC ratio of C3 and adipsin with increasing BMI. These results suggest that in female SC adipose tissue, there is downregulation of factors related to ASP production in obesity, perhaps to limit further expansion of adipose tissue. In males, there is increased expression in OM tissue. In addition, relative OM/SC expression increases with obesity and these changes may contribute to the development of visceral adipose tissue.     

二甲双胍对糖尿病前期患者生长分化因子15及体脂分布影响的研究

目的探讨二甲双胍对DM前期患者生长分化因子15(GDF-15)及体脂分布的影响。方法选取DM前期患者112例,随机分为标准生活方式干预+二甲双胍的试验组(Exp)和仅标准生活方式干预的对照组(Con),每组各56例。干预1年后比较两组体重、BMI、WC、体脂分布、血糖、Ins、GDF-15等指标变化。再以BMI≥24 kg/m²为标准分为超重/肥胖组和体重正常组,多元线性回归分析GDF-15的影响因素。结果干预1年后Exp组FPG、2 h PG低于Con组(P<0.05),定量IS指数(QUICKI)、GDF-15高于Con组(P<0.05);超重/肥胖组TC、TG、HbA₁c、2 h Ins、WC、内脏脂肪面积、四肢、A区及G区脂肪质量较前降低(P<0.05),GDF-15较前升高(P<0.05)。Spearman相关分析显示,GDF-15与年龄、QUICKI呈正相关(r=0.362、0.375,P<0.05),与FIns呈负相关(r=-0.353,P<0.05)。多元线性回归分析显示,应用二甲双胍是GDF-15的影响因素,应用二甲双胍是A区脂肪质量的影响因素。结论二甲双胍干预可减少DM前期患者腹部脂肪,升高GDF-15,且在超重/肥胖人群更显著。     

White adipose tissue mitochondrial metabolism in health and in obesity

White adipose tissue is one of the largest organs of the body. It plays a key role in whole‐body energy status and metabolism; it not only stores excess energy but also secretes various hormones and metabolites to regulate body energy balance. Healthy adipose tissue capable of expanding is needed for metabolic well‐being and to prevent accumulation of triglycerides to other organs. Mitochondria govern several important functions in the adipose tissue. We review the derangements of mitochondrial function in white adipose tissue in the obese state. Downregulation of mitochondrial function or biogenesis in the white adipose tissue is a central driver for obesity‐associated metabolic diseases. Mitochondrial functions compromised in obesity include oxidative functions and renewal and enlargement of the adipose tissue through recruitment and differentiation of adipocyte progenitor cells. These changes adversely affect whole‐body metabolic health. Dysfunction of the white adipose tissue mitochondria in obesity has long‐term consequences for the metabolism of adipose tissue and the whole body. Understanding the pathways behind mitochondrial dysfunction may help reveal targets for pharmacological or nutritional interventions that enhance mitochondrial biogenesis or function in adipose tissue.