scholarly journals Serum Antioxidant Associations with Metabolic Characteristics in Metabolically Healthy and Unhealthy Adolescents with Severe Obesity: An Observational Study

Nutrients ◽  
2018 ◽  
Vol 10 (2) ◽  
pp. 150 ◽  
Author(s):  
Ana Stenzel ◽  
Roberta Carvalho ◽  
Patricia Jesus ◽  
Aline Bull ◽  
Silvia Pereira ◽  
...  
Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Lance C Dalleck ◽  
Tara B Richardson ◽  
Gary P Van Guilder

Introduction: It has been estimated that 32% of obese adults in the US are metabolically healthy. This subset of individuals, referred to as metabolically healthy but obese (MHO), appear to be more resistant to the adverse cardiometabolic consequences faced by their metabolically abnormal obese (MAO) counterparts. Cross-sectional observations indicate that increased physical activity and higher fitness contribute to the protective metabolic characteristics in this subset of obese individuals. However, to date no study has investigated whether a community-based exercise intervention designed to increase exercise volume and fitness can transition MAO adults to a MHO phenotype. Identifying the therapeutic dose of exercise required to convert a MAO person to metabolically healthy would yield important clinical information for the primary prevention of cardiovascular disease. Hypothesis: We assessed the following hypotheses: (1) community-based exercise training would transition MAO adults to metabolically healthy, and (2) the odds of successful transition to a metabolically healthy phenotype would be larger for obese individuals who [[Unable to Display Character: &#8211;]] (a) performed the highest volume of exercise, and (b) experienced the greatest increase in fitness. Methods: Three-hundred thirty-two healthy adults (190 women, 142 men; aged 28-88 years) engaged in a supervised 14-week community-based exercise program designed to favorably modify cardiovascular disease risk factors. Components of the metabolic syndrome (National Cholesterol Education Program ATP III criteria) were measured before and after the exercise program. Obese (BMI ≥ 30 kg·m 2 ) adults who met 2-4 criteria for metabolic syndrome were classified as metabolically abnormal. Metabolically healthy was defined if obese adults met 0 to 1 criteria for metabolic syndrome. Results: Baseline point prevalence of MAO was 20.5% (N = 68). There was a significant reduction (p<0.05) in point prevalence of MAO to 12.3% by post program as 27/68 individuals (40%) transitioned to MHO. Compared to the lowest quartiles of relative energy expenditure and change in fitness, participants in the highest quartiles were 21.8 (95% CI 4.4[[Unable to Display Character: &#8211;]]108.0; p<0.05) and 8.2 (95% CI 3.1[[Unable to Display Character: &#8211;]]21.6; p<0.05) times more likely to transition from MAO to MHO, respectively. Conclusions: These findings indicate that supervised community exercise can transition MAO adults to a MHO phenotype. MAO adults who engaged in higher volumes of exercise and those who demonstrated greater improvements in fitness were significantly more likely to become metabolically healthy. Importantly, the unfavourable metabolic characteristics of obesity are not irreversible. Community exercise should be considered an effective model for the primary prevention of cardiovascular disease in MAO adults.


2020 ◽  
Vol Volume 13 ◽  
pp. 197-205 ◽  
Author(s):  
Mohammed F Rafey ◽  
Conor F Murphy ◽  
Razk Abdalgwad ◽  
Katriona Kilkelly ◽  
Helena Griffin ◽  
...  

2013 ◽  
Vol 34 (1) ◽  
pp. 19 ◽  
Author(s):  
Ho Kwon Yoo ◽  
Eun Young Choi ◽  
Eal Whan Park ◽  
Yoo-Seock Cheong ◽  
Ri Ah Bae

2009 ◽  
Vol 425 (1) ◽  
pp. 71-85 ◽  
Author(s):  
Fangnian Wang ◽  
Hongsheng Liu ◽  
Wanda P. Blanton ◽  
Anna Belkina ◽  
Nathan K. Lebrasseur ◽  
...  

Certain human subpopulations are metabolically healthy but obese, or metabolically obese but normal weight; such mutations uncouple obesity from glucose intolerance, revealing pathways implicated in Type 2 diabetes. Current searches for relevant genes consume significant effort. We have reported previously a novel double bromodomain protein called Brd2, which is a transcriptional co-activator/co-repressor with SWI/SNF (switch mating type/sucrose non-fermenting)-like functions that regulates chromatin. In the present study, we show that wholebody disruption of Brd2, an unusual MHC gene, causes lifelong severe obesity in mice with pancreatic islet expansion, hyperinsulinaemia, hepatosteatosis and elevated pro-inflammatory cytokines, but, surprisingly, enhanced glucose tolerance, elevated adiponectin, increased weight of brown adipose tissue, heat production and expression of mitochondrial uncoupling proteins in brown adipose tissue, reduced macrophage infiltration in white adipose tissue, and lowered blood glucose, leading to an improved metabolic profile and avoiding eventual Type 2 diabetes. Brd2 is highly expressed in pancreatic β-cells, where it normally inhibits β-cell mitosis and insulin transcription. In 3T3-L1 pre-adipocytes, Brd2 normally co-represses PPAR-γ (peroxisome-proliferator-activated receptor-γ) and inhibits adipogenesis. Brd2 knockdown protects 3T3-L1 adipocytes from TNF-α (tumour necrosis factor-α)-induced insulin resistance, thereby decoupling inflammation from insulin resistance. Thus hypomorphic Brd2 shifts energy balance toward storage without causing glucose intolerance and may provide a novel model for obese metabolically healthy humans.


2020 ◽  
Vol 134 (18) ◽  
pp. 2447-2451
Author(s):  
Anissa Viveiros ◽  
Gavin Y. Oudit

Abstract The global prevalence of obesity has been rising at an alarming rate, accompanied by an increase in both childhood and maternal obesity. The concept of metabolic programming is highly topical, and in this context, describes a predisposition of offspring of obese mothers to the development of obesity independent of environmental factors. Research published in this issue of Clinical Science conducted by Litzenburger and colleagues (Clin. Sci. (Lond.) (2020) 134, 921–939) have identified sex-dependent differences in metabolic programming and identify putative signaling pathways involved in the differential phenotype of adipose tissue between males and females. Delineating the distinction between metabolically healthy and unhealthy obesity is a topic of emerging interest, and the precise nature of adipocytes are key to pathogenesis, independent of adipose tissue volume.


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