scholarly journals Targeting White Adipose Tissue with Exercise or Bariatric Surgery as Therapeutic Strategies in Obesity

Biology ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 16 ◽  
Author(s):  
Flávia Giolo De Carvalho ◽  
Lauren Sparks
Keyword(s):  
Bariatric Surgery ◽  
Adipose Tissue ◽  
Resistance Exercise ◽  
Treatment Strategies ◽  
Whole Body ◽  
Metabolic Complications ◽  
Bona Fide ◽  
Treatment Of Obesity ◽  
Exercise Induced ◽  
The Impact

Adipose tissue is critical to whole-body energy metabolism and has become recognized as a bona fide endocrine organ rather than an inert lipid reservoir. As such, adipose tissue is dynamic in its ability to secrete cytokines, free fatty acids, lipokines, hormones and other factors in response to changes in environmental stimuli such as feeding, fasting and exercise. While excess adipose tissue, as in the case of obesity, is associated with metabolic complications, mass itself is not the only culprit in obesity-driven metabolic abnormalities, highlighting the importance of healthy and metabolically adaptable adipose tissue. In this review, we discuss the fundamental cellular processes of adipose tissue that become perturbed in obesity and the impact of exercise on these processes. While both endurance and resistance exercise can promote positive physiological adaptations in adipose tissue, endurance exercise has a more documented role in remodeling adipocytes, increasing adipokine secretion and fatty acid mobilization and oxidation during post-exercise compared with resistance exercise. Exercise is considered a viable therapeutic strategy for the treatment of obesity to optimize body composition, in particular as an adjuvant therapy to bariatric surgery; however, there is a gap in knowledge of the molecular underpinnings of these exercise-induced adaptations, which could provide more insight and opportunity for precision-based treatment strategies.

scholarly journals Weight Status and Visceral Adiposity Mediate the Relationship between Exclusive Breastfeeding Duration and Skin Carotenoids in Later Childhood

2021 ◽  
Author(s):  
Ruyu Liu ◽  
Caitlyn G Edwards ◽  
Corinne N Cannavale ◽  
Isabel R Flemming ◽  
Morgan R Chojnacki ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Exclusive Breastfeeding ◽  
Weight Status ◽  
Mediating Effect ◽  
Physical Growth ◽  
Breastfeeding Duration ◽  
Whole Body ◽  
Controlled Clinical Trial ◽  
The Impact ◽  
The Relationship

Abstract Background Breastfeeding is associated with healthier weight and nutrient status in early life. However, the impact of breastfeeding on carotenoid status beyond infancy, and the influence of adiposity, is unknown. Objective The aim of the study was to retrospectively investigate the relationship between breastfeeding and carotenoid status, and the mediating effect of weight status and adiposity on this relationship among school-aged children. Methods This was a secondary analysis of baseline data collected from a randomized-controlled clinical trial. (ClinicalTrials.gov Identifier: NCT03521349). 7–12-year-old (n = 81) children were recruited from East-Central Illinois. Dual-energy x-ray absorptiometry (DXA) was used to assess visceral adipose tissue (VAT) and whole-body adiposity (%Fat). Weight was obtained to calculated body mass index percentile (BMI %ile). Skin carotenoids were assessed via reflection spectroscopy. Macular carotenoids were assessed as macular pigment optical density (MPOD). Dietary, birth, and breastfeeding information was self-reported by parents. Results Skin carotenoids were inversely related to %Fat (P < 0.01), VAT (P < 0.01) and BMI %ile (P < 0.01). VAT and BMI %ile significantly mediated this relationship between exclusive breastfeeding duration and skin carotenoids, following adjustment for dietary carotenoids, energy intake, and mother education. Conclusions Weight status and adipose tissue distribution mediate the positive correlation between exclusive breastfeeding duration and skin carotenoids among children aged 7–12 years. The results indicate the need to support breastfeeding and healthy physical growth in childhood for optimal carotenoid status.

Inflammation and impaired adipogenesis in hypertrophic obesity in man

2009 ◽  
Vol 297 (5) ◽  
pp. E999-E1003 ◽  
Author(s):  
Birgit Gustafson ◽  
Silvia Gogg ◽  
Shahram Hedjazifar ◽  
Lachmi Jenndahl ◽  
Ann Hammarstedt ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Molecular Mechanisms ◽  
Whole Body ◽  
Preadipocyte Differentiation ◽  
Metabolic Complications ◽  
Adipose Cell ◽  
Subcutaneous Adipose ◽  
Adipose Cell Size

Obesity is associated mainly with adipose cell enlargement in adult man (hypertrophic obesity), whereas the formation of new fat cells (hyperplastic obesity) predominates in the prepubertal age. Adipose cell size, independent of body mass index, is negatively correlated with whole body insulin sensitivity. Here, we review recent findings linking hypertrophic obesity with inflammation and a dysregulated adipose tissue, including local cellular insulin resistance with reduced IRS-1 and GLUT4 protein content. In addition, the number of preadipocytes in the abdominal subcutaneous adipose tissue capable of undergoing differentiation to adipose cells is reduced in hypertrophic obesity. This is likely to promote ectopic lipid accumulation, a well-known finding in these individuals and one that promotes insulin resistance and cardiometabolic risk. We also review recent results showing that TNFα, but not MCP-1, resistin, or IL-6, completely prevents normal adipogenesis in preadipocytes, activates Wnt signaling, and induces a macrophage-like phenotype in the preadipocytes. In fact, activated preadipocytes, rather than macrophages, may completely account for the increased release of chemokines and cytokines by the adipose tissue in obesity. Understanding the molecular mechanisms for the impaired preadipocyte differentiation in the subcutaneous adipose tissue in hypertrophic obesity is a priority since it may lead to new ways of treating obesity and its associated metabolic complications.

Resistance training reduces whole-body protein turnover and improves net protein retention in untrained young males

2006 ◽  
Vol 31 (5) ◽  
pp. 557-564 ◽  
Author(s):  
Joseph W. Hartman ◽  
Daniel R. Moore ◽  
Stuart M. Phillips
Keyword(s):  
Resistance Training ◽  
Resistance Exercise ◽  
Nitrogen Balance ◽  
Protein Turnover ◽  
Whole Body ◽  
Body Protein ◽  
Protein Retention ◽  
The Impact ◽  
Net Protein ◽  
Urinary Nitrogen

It is thought that resistance exercise results in an increased need for dietary protein; however, data also exists to support the opposite conclusion. The purpose of this study was to determine the impact of resistance exercise training on protein metabolism in novices with the hypothesis that resistance training would reduce protein turnover and improve whole-body protein retention. Healthy males (n = 8, 22 ± 1 y, BMI = 25.3 ± 1.8 kg·m–2) participated in a progressive whole-body split routine resistance-training program 5d/week for 12 weeks. Before (PRE) and after (POST) the training, oral [15N]-glycine ingestion was used to assess nitrogen flux (Q), protein synthesis (PS), protein breakdown (PB), and net protein balance (NPB = PS – PB). Macronutrient intake was controlled over a 5d period PRE and POST, while estimates of protein turnover and urinary nitrogen balance (Nbal = Nin – urine Nout) were conducted. Bench press and leg press increased 40% and 50%, respectively (p < 0.01). Fat- and bone-free mass (i.e., lean muscle mass) increased from PRE to POST (2.5 ± 0.8 kg, p < 0.05). Significant PRE to POST decreases (p <0.05) occurred in Q (0.9 ± 0.1 vs. 0.6 ± 0.1 g N·kg–1·d–1), PS (4.6 ± 0.7 vs. 2.9 ± 0.3 g·kg–1·d–1), and PB (4.3 ± 0.7 vs. 2.4 ± 0.2 g·kg–1·d–1). Significant training-induced increases in both NPB (PRE = 0.22 ± 0.13 g·kg–1·d–1; POST = 0.54 ± 0.08 g·kg–1·d–1) and urinary nitrogen balance (PRE = 2.8 ± 1.7 g N·d–1; POST = 6.5 ± 0.9 g N·d–1) were observed. A program of resistance training that induced significant muscle hypertrophy resulted in reductions of both whole-body PS and PB, but an improved NPB, which favoured the accretion of skeletal muscle protein. Urinary nitrogen balance increased after training. The reduction in PS and PB and a higher NPB in combination with an increased nitrogen balance after training suggest that dietary requirements for protein in novice resistance-trained athletes are not higher, but lower, after resistance training.

scholarly journals Mechanisms of Insulin Action and Insulin Resistance

2018 ◽  
Vol 98 (4) ◽  
pp. 2133-2223 ◽  
Author(s):  
Max C. Petersen ◽  
Gerald I. Shulman
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Insulin Action ◽  
Big Bang ◽  
Whole Body ◽  
Detailed Knowledge ◽  
Bioactive Lipids ◽  
Mechanistic Investigation ◽  
The Impact

The 1921 discovery of insulin was a Big Bang from which a vast and expanding universe of research into insulin action and resistance has issued. In the intervening century, some discoveries have matured, coalescing into solid and fertile ground for clinical application; others remain incompletely investigated and scientifically controversial. Here, we attempt to synthesize this work to guide further mechanistic investigation and to inform the development of novel therapies for type 2 diabetes (T2D). The rational development of such therapies necessitates detailed knowledge of one of the key pathophysiological processes involved in T2D: insulin resistance. Understanding insulin resistance, in turn, requires knowledge of normal insulin action. In this review, both the physiology of insulin action and the pathophysiology of insulin resistance are described, focusing on three key insulin target tissues: skeletal muscle, liver, and white adipose tissue. We aim to develop an integrated physiological perspective, placing the intricate signaling effectors that carry out the cell-autonomous response to insulin in the context of the tissue-specific functions that generate the coordinated organismal response. First, in section II, the effectors and effects of direct, cell-autonomous insulin action in muscle, liver, and white adipose tissue are reviewed, beginning at the insulin receptor and working downstream. Section III considers the critical and underappreciated role of tissue crosstalk in whole body insulin action, especially the essential interaction between adipose lipolysis and hepatic gluconeogenesis. The pathophysiology of insulin resistance is then described in section IV. Special attention is given to which signaling pathways and functions become insulin resistant in the setting of chronic overnutrition, and an alternative explanation for the phenomenon of ‟selective hepatic insulin resistanceˮ is presented. Sections V, VI, and VII critically examine the evidence for and against several putative mediators of insulin resistance. Section V reviews work linking the bioactive lipids diacylglycerol, ceramide, and acylcarnitine to insulin resistance; section VI considers the impact of nutrient stresses in the endoplasmic reticulum and mitochondria on insulin resistance; and section VII discusses non-cell autonomous factors proposed to induce insulin resistance, including inflammatory mediators, branched-chain amino acids, adipokines, and hepatokines. Finally, in section VIII, we propose an integrated model of insulin resistance that links these mediators to final common pathways of metabolite-driven gluconeogenesis and ectopic lipid accumulation.

scholarly journals Metabolic Effects of Bariatric Surgery

2018 ◽  
Vol 64 (1) ◽  
pp. 72-81 ◽  
Author(s):  
Piriyah Sinclair ◽  
Neil Docherty ◽  
Carel W le Roux
Keyword(s):  
Type 2 Diabetes ◽  
Bariatric Surgery ◽  
Metabolic Surgery ◽  
Positive Impact ◽  
Metabolic Effects ◽  
Beneficial Effects ◽  
Treatment Of Obesity ◽  
The Impact ◽  
The Brain

Abstract BACKGROUND Obesity can be defined as a chronic subcortical brain disease, as there is an important neurophysiological component to its etiology based on changes in the functioning of those areas of the brain controlling food intake and reward. Extensive metabolic changes accompany bariatric surgery-based treatment of obesity. Consequently, the term “metabolic” surgery is being increasingly adopted in relation to the beneficial effects these procedures have on chronic diseases like type 2 diabetes. CONTENT In the present review, we focus on the key biochemical and physiological changes induced by metabolic surgery and highlight the beneficial effects accrued systemically with the use of an organ-based approach. Understanding the impact on and interactions between the gut, brain, adipose tissue, liver, muscle, pancreas, and kidney is key to understanding the sum of the metabolic effects of these operations. SUMMARY Further mechanistic studies are essential to assess the true potential of metabolic surgery to treat metabolic comorbidities of obesity beyond type 2 diabetes. Approaches that may mitigate the metabolic side effects of surgery also require attention. Understanding the positive impact of metabolic surgery on metabolic health may result in a wider acceptance of this intervention as treatment for metabolic, comorbid conditions.

scholarly journals Influenza infection rewires energy metabolism and induces browning features in adipose cells and tissues

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Asma Ayari ◽  
Manuel Rosa-Calatrava ◽  
Steve Lancel ◽  
Johanna Barthelemy ◽  
Andrés Pizzorno ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Influenza A ◽  
Energy Homeostasis ◽  
Influenza Infection ◽  
Subcutaneous Fat ◽  
Whole Body ◽  
Glucose And Lipid Metabolism ◽  
The Impact

AbstractLike all obligate intracellular pathogens, influenza A virus (IAV) reprograms host cell’s glucose and lipid metabolism to promote its own replication. However, the impact of influenza infection on white adipose tissue (WAT), a key tissue in the control of systemic energy homeostasis, has not been yet characterized. Here, we show that influenza infection induces alterations in whole-body glucose metabolism that persist long after the virus has been cleared. We report depot-specific changes in the WAT of IAV-infected mice, notably characterized by the appearance of thermogenic brown-like adipocytes within the subcutaneous fat depot. Importantly, viral RNA- and viral antigen-harboring cells are detected in the WAT of infected mice. Using in vitro approaches, we find that IAV infection enhances the expression of brown-adipogenesis-related genes in preadipocytes. Overall, our findings shed light on the role that the white adipose tissue, which lies at the crossroads of nutrition, metabolism and immunity, may play in influenza infection.

Diet, obesity and diabetes: a current update

2006 ◽  
Vol 112 (2) ◽  
pp. 93-111 ◽  
Author(s):  
Celia G. Walker ◽  
M. Gulrez Zariwala ◽  
Mark J. Holness ◽  
Mary C. SUGDEN
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Energy Balance ◽  
Whole Body ◽  
Primary Defect ◽  
Obesity And Diabetes ◽  
Tissue Factors ◽  
Metabolic Conditions ◽  
The Impact

The prevalence of obesity has been increasing at a rapid rate over the last few decades. Although the primary defect can be attributed to an imbalance of energy intake over energy expenditure, the regulation of energy balance is now recognized to be complex. Adipose-tissue factors play a central role in the control of energy balance and whole-body fuel homoeostasis. The regulation of adipose-tissue function, in particular its secretion of adipokines, is impaired by increases in adipose mass associated with obesity, and with the development of insulin resistance and Type 2 diabetes. This review analyses adipose-regulated energy input and expenditure, together with the impact of dietary macronutrient composition on energy balance in relation to susceptibility to the development of obesity and Type 2 diabetes, and how these metabolic conditions may be exacerbated by the consequences of abnormal adipose function. By gaining a greater understanding of how energy balance is controlled in normal, and in obese and diabetic states, a more practical approach can be employed to prevent and better treat obesity and metabolic disorders.

Lipid mobilization in subcutaneous adipose tissue during exercise in lean and obese humans. Roles of insulin and natriuretic peptides

2010 ◽  
Vol 299 (2) ◽  
pp. E258-E265 ◽  
Author(s):  
Katrien Koppo ◽  
Dominique Larrouy ◽  
Marie A. Marques ◽  
Michel Berlan ◽  
Magda Bajzova ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Exercise Bout ◽  
Saline Control ◽  
Microdialysis Probe ◽  
Lipid Mobilization ◽  
Obese Subjects ◽  
Exercise Induced ◽  
Subcutaneous Adipose ◽  
The Impact

The aim of this study was to evaluate the relative contributions of various hormones involved in the regulation of lipid mobilization in subcutaneous adipose tissue (SCAT) during exercise and to assess the impact of obesity on this regulation. Eight lean and eight obese men performed a 60-min cycle exercise bout at 50% of their peak oxygen uptake on two occasions: during intravenous infusion of octreotide (a somatostatin analog) or physiological saline (control condition). Lipolysis in SCAT was evaluated using in situ microdialysis. One microdialysis probe was perfused with the adrenergic blockers phentolamine and propranolol while another probe was perfused with the phosphodiesterase and adenosine receptor inhibitor aminophylline. Compared with the control condition, infusion of octreotide reduced plasma insulin levels in lean (from ∼3.5 to 0.5 μU/ml) and in obese (from ∼9 to 2 μU/ml), blunted the exercise-induced rise in plasma GH and epinephrine levels in both groups, and enhanced the exercise-induced natriuretic peptide (NP) levels in lean but not in obese subjects. In both groups, octreotide infusion resulted in higher exercise-induced increases in dialysate glycerol concentrations in the phentolamine-containing probe while no difference in lipolytic response was found in the aminophylline-containing probe. The results suggest that insulin antilipolytic action plays a role in the regulation of lipolysis during exercise in lean as well as in obese subjects. The octreotide-induced enhancement of exercise lipolysis in lean subjects was associated with an increased exercise-induced plasma NP response. Adenosine may contribute to the inhibition of basal lipolysis in both subject groups.

Sign in / Sign up

Export Citation Format

Share Document