scholarly journals Effects of magnitude of visceral adipose tissue reduction: Impact on insulin resistance, hyperleptinemia and cardiometabolic risk in adolescents with obesity after long-term weight-loss therapy

2019 ◽  
Vol 16 (2) ◽  
pp. 196-206 ◽  
Author(s):  
Raquel Munhoz da Silveira Campos ◽  
Deborah Cristina Landi Masquio ◽  
Flávia Campos Corgosinho ◽  
Danielle Arisa Caranti ◽  
Aline de Piano Ganen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Visceral Fat ◽  
Independent Predictor ◽  
Fat Reduction ◽  
Visceral Adipose ◽  
Weight Loss Therapy

Aim: To investigate the association between visceral adipose tissue loss and insulin resistance and hyperleptinemia in adolescents with obesity submitted to interdisciplinary weight-loss therapy. Methods: A total of 172 post-pubertal adolescents (body mass index greater than the 95th percentile of the Centers for Disease Control and Prevention reference growth charts) were recruited for the study. The adolescents were assigned to long-term weight-loss therapy. Body composition, visceral and subcutaneous fat, glucose metabolism, lipid profile, hepatic enzymes and leptin concentration were measured. After the therapy, the adolescents were allocated to three different groups according to the tertile of visceral fat reduction. Results: Positive effects on body composition were observed in all analysed groups independent of visceral fat reduction. It was found that visceral fat was an independent predictor of insulin resistance in the investigated population. Obese adolescents who lost a higher proportion of visceral adipose tissue (>1.8 cm) demonstrated improved metabolic and inflammatory parameters twice as much than those who presented smaller losses. Positive correlations between visceral fat reduction and glucose metabolism, lipid profile, hepatic enzymes and homeostasis model assessment of insulin resistance index were demonstrated. Conclusion: The magnitude of the reduction in visceral fat was an independent predictor of insulin resistance, hyperleptinemia and metabolic disorders related to obese adolescents.

scholarly journals The effect of caloric restriction on the increase in senescence-associated T cells and metabolic disorders in aged mice

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252547
Author(s):  
Xiaoxiang Yan ◽  
Natsumi Imano ◽  
Kayoko Tamaki ◽  
Motoaki Sano ◽  
Ken Shinmura
Keyword(s):  
Insulin Resistance ◽  
T Cells ◽  
Adipose Tissue ◽  
T Cell ◽  
Caloric Restriction ◽  
Visceral Adipose Tissue ◽  
Aged Mice ◽  
Age Related ◽  
Visceral Adipose

Aging is associated with functional decline in the immune system and increases the risk of chronic diseases owing to smoldering inflammation. In the present study, we demonstrated an age-related increase in the accumulation of Programmed Death-1 (PD-1)+ memory-phenotype T cells that are considered “senescence-associated T cells” in both the visceral adipose tissue and spleen. As caloric restriction is an established intervention scientifically proven to exert anti-aging effects and greatly affects physiological and pathophysiological alterations with advanced age, we evaluated the effect of caloric restriction on the increase in this T-cell subpopulation and glucose tolerance in aged mice. Long-term caloric restriction significantly decreased the number of PD-1+ memory-phenotype cluster of differentiation (CD) 4+ and CD8+ T cells in the spleen and visceral adipose tissue, decreased M1-type macrophage accumulation in visceral adipose tissue, and improved insulin resistance in aged mice. Furthermore, the immunological depletion of PD-1+ T cells reduced adipose inflammation and improved insulin resistance in aged mice. Taken together with our previous report, these results indicate that senescence-related T-cell subpopulations are involved in the development of chronic inflammation and insulin resistance in the context of chronological aging and obesity. Thus, long-term caloric restriction and specific deletion of senescence-related T cells are promising interventions to regulate age-related chronic diseases.

scholarly journals Metabolically healthy obesity: what's in a name?

2019 ◽  
Vol 110 (3) ◽  
pp. 533-539 ◽  
Author(s):  
Faidon Magkos
Keyword(s):  
Weight Loss ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Visceral Adipose Tissue ◽  
Liver Fat ◽  
Metabolically Healthy Obesity ◽  
Liver Fat Content ◽  
Metabolically Healthy ◽  
Visceral Adipose

ABSTRACT Metabolically healthy obesity refers to an obesity phenotype with no or little evidence of metabolic dysfunction. Lower liver fat content and visceral adipose tissue, greater insulin sensitivity and secretion, greater cardiorespiratory fitness, and a predominantly lower body (i.e., leg) fat deposition are key physiological traits of a metabolically healthy phenotype. About 35% of all subjects with obesity are metabolically healthy. These individuals have approximately half the risk of developing type 2 diabetes and cardiovascular disease compared with metabolically unhealthy subjects with obesity, but they still have a significantly greater risk (by 50–300%) compared with metabolically healthy lean subjects. Therefore, absence of metabolic risk factors in people with obesity should not be a contraindication for weight-loss treatment. Metabolically healthy obesity needs to be treated, and this need is reinforced by the fact that this phenotype is not stable over time, as ∼50% of these subjects will cease being metabolically healthy within ∼10 y. Intervening early is therefore important. Weight loss dose-dependently decreases visceral adipose tissue and liver fat content, and it improves multiorgan insulin sensitivity and β-cell function (i.e., it beneficially affects many of the physiological traits of a metabolically healthy phenotype); however, weight loss is very difficult to maintain. This typically results in disappointment among patients and hinders adherence, which is likely critical for the limited success of most weight-loss treatments in the long term. On the other hand, using ≥1 metabolic health targets in a non-weight-loss-centered treatment paradigm that includes prudent dietary changes and increased physical activity can serve as an appropriate first goal that can help motivate patients toward the long-term goals of obesity treatment.

scholarly journals Oxidative modifications of mitochondrial complex II are associated with insulin resistance of visceral fat in obesity

2019 ◽  
Vol 316 (2) ◽  
pp. E168-E177 ◽  
Author(s):  
Doan T. M. Ngo ◽  
Aaron L. Sverdlov ◽  
Shakun Karki ◽  
Donia Macartney-Coxson ◽  
Richard S. Stubbs ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Bariatric Surgery ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Insulin Treatment ◽  
Subcutaneous Fat ◽  
Mitochondrial Complex ◽  
Complex Ii ◽  
Visceral Adipose

Obesity, particularly visceral adiposity, has been linked to mitochondrial dysfunction and increased oxidative stress, which have been suggested as mechanisms of insulin resistance. The mechanism(s) behind this remains incompletely understood. In this study, we hypothesized that mitochondrial complex II dysfunction plays a role in impaired insulin sensitivity in visceral adipose tissue of subjects with obesity. We obtained subcutaneous and visceral adipose tissue biopsies from 43 subjects with obesity (body mass index ≥ 30 kg/m2) during planned bariatric surgery. Compared with subcutaneous adipose tissue, visceral adipose tissue exhibited decreased complex II activity, which was restored with the reducing agent dithiothreitol (5 mM) ( P < 0.01). A biotin switch assay identified that cysteine oxidative posttranslational modifications (OPTM) in complex II subunit A (succinate dehydrogenase A) were increased in visceral vs. subcutaneous fat ( P < 0.05). Insulin treatment (100 nM) stimulated complex II activity in subcutaneous fat ( P < 0.05). In contrast, insulin treatment of visceral fat led to a decrease in complex II activity ( P < 0.01), which was restored with addition of the mitochondria-specific oxidant scavenger mito-TEMPO (10 µM). In a cohort of 10 subjects with severe obesity, surgical weight loss decreased OPTM and restored complex II activity, exclusively in the visceral depot. Mitochondrial complex II may be an unrecognized and novel mediator of insulin resistance associated with visceral adiposity. The activity of complex II is improved by weight loss, which may contribute to metabolic improvements associated with bariatric surgery.

Gain without pain: beyond sport effortless exercise solutions

2020 ◽  
Vol 9 (5) ◽  
pp. 202-210
Author(s):  
Xanya Sofra
Keyword(s):  
Weight Loss ◽  
Adipose Tissue ◽  
Metabolic Rate ◽  
Body Fat ◽  
Fat Mass ◽  
Visceral Adipose Tissue ◽  
Visceral Fat ◽  
Body Fat Mass ◽  
Free T3 ◽  
Visceral Adipose

Ageing is associated with decreased metabolism, increased toxicity, decreased skeletal muscle mass (SMM) and increased visceral fat deposits that compromise the normal functioning of vital organs such as the liver, pancreas and intestines, increasing the risk of a number of health problems, including type 2 diabetes, coronary heart disease, hypertension and non-alcoholic fatty liver. Visceral adipose tissue holds large amounts of toxins that alter thyroid hormone metabolism, lowering resting metabolic rate (RMR). Strenuous physical exercise can reach these deeper visceral adipose tissue layers. However, excessive exercise is necessary to reduce visceral adipose tissue elevates cortisol while decreasing testosterone. The hormonal imbalance resulting from this inverse cortisol/testosterone relationship ultimately leads to weight gain, despite all the efforts invested in physical activity. On the other hand, lack of exercise allows for accumulation of toxicity and increased vulnerability to chronic physical disorders. Energy-based technologies report successful results in reducing subcutaneous fat layers; however, data is not currently available about methods that can reduce deeper visceral adipose tissue and relieve the system from visceral fat cells stuffed with excess triglycerides. In this study, we examined hormone and cholesterol fluctuations in the blood tests of eight subjects undergoing six 45 minutes of effortless exercise sessions with a novel London University invention. We also explored changes in their visceral adipose tissue, overall body fat mass, SMM, basic metabolic rate (BMR), waist and abdomen reduction in centimetres (cm) and overall weight loss in kilograms (kg). Subjects' results revealed a statistically significant increase in triiodothyronine (Free T3), accompanied by a significant decrease in the very low-density lipoprotein (VLDL) and triglycerides. Cortisol did not show statistically significant fluctuations. There was a statistically significant decrease in visceral adipose tissue and overall body fat mass and a statistically significant increase in SMM. Waist and abdomen cm loss, and weight loss in kgs were statistically significant, demonstrating a substantial decrease in cm and kgs in all subjects that persisted a week after the last treatment. Results of this study supported the hypothesis that this method of effortless exercise can reduce both overall body fat mass, visceral adipose tissue and VLDL, while increasing SMM and the metabolic hormone free T3, without the aid of diet or change in lifestyle.

scholarly journals Worsening of Obesity and Metabolic Status Yields Similar Molecular Adaptations in Human Subcutaneous and Visceral Adipose Tissue: Decreased Metabolism and Increased Immune Response

Endocrinology ◽  
2010 ◽  
Vol 151 (12) ◽  
pp. 5972-5972
Author(s):  
Eva Klimčáková ◽  
Balbine Roussel ◽  
Adriana Márquez-Quiñones ◽  
Zuzana Kováčová ◽  
Michaela Kováčiková ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Immune Response ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Visceral Fat ◽  
Down Regulation ◽  
Immune Response Genes ◽  
Visceral Adipose

Context: It is not known whether biological differences reported between sc adipose tissue (SAT) and visceral adipose tissue (VAT) depots underlie the pathogenicity of visceral fat. Objective: We compared SAT and VAT gene expression according to obesity, visceral fat accumulation, insulin resistance, and presence of the metabolic syndrome. Design: Subjects were assigned into four groups (lean, overweight, obese, and obese with metabolic syndrome). Setting: Subjects were recruited at a university hospital. Patients: Thirty-two women were included. Main Outcome Measures: Anthropometric measurements, euglycemic-hyperinsulinemic clamps, blood analyses, and computed tomography scans were performed, and paired samples of SAT and VAT were obtained for DNA microarray-based gene expression profiling. Results: Considering the two fat depots together, 1125 genes were more and 1025 genes were less expressed in lean compared with metabolic syndrome subjects. Functional annotation clustering showed, from lean to metabolic syndrome subjects, progressive down-regulation of metabolic pathways including branched-chain amino acid, fatty acid, carbohydrate, and mitochondrial energy metabolism and up-regulation of immune response genes involved in toll-like receptor, TNF, nuclear factor-κB, and apoptosis pathways. Metabolism and immune response genes showed an opposite correlation with fat mass, fat distribution, or insulin resistance indices. These associations were similar in SAT and VAT, although about 1000 genes showed differential expression between SAT and VAT. Conclusions: The increase in adiposity and the worsening of metabolic status are associated with a coordinated down-regulation of metabolism-related and up-regulation of immune response-related gene expression. Molecular adaptations in SAT prove as discriminating as those in VAT.

scholarly journals Effect of Long-Term Whole Body Vibration Training on Visceral Adipose Tissue: A Preliminary Report

Obesity Facts ◽  
2010 ◽  
Vol 3 (2) ◽  
pp. 7-7 ◽  
Author(s):  
Dirk Vissers ◽  
An Verrijken ◽  
Ilse Mertens ◽  
Caroline Van Gils ◽  
Annemie Van de Sompel ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Preliminary Report ◽  
Whole Body Vibration ◽  
Whole Body ◽  
Body Vibration ◽  
Vibration Training ◽  
Whole Body Vibration Training ◽  
Visceral Adipose

scholarly journals Elevated serum uric acid is a facilitating mechanism for insulin resistance mediated accumulation of visceral adipose tissue

2020 ◽  
Author(s):  
Luisa Fernández-Chirino ◽  
Neftali Eduardo Antonio-Villa ◽  
Arsenio Vargas-Vázquez ◽  
Paloma Almeda-Valdés ◽  
Donají Gómez-Velasco ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Uric Acid ◽  
Serum Uric Acid ◽  
Visceral Adipose Tissue ◽  
Visceral Obesity ◽  
Causal Mechanism ◽  
Mediation Analyses ◽  
Bidirectional Relationship ◽  
Visceral Adipose

BACKGROUND: Serum uric acid (SUA) has a relationship with cardiometabolic conditions such as insulin resistance (IR) and visceral adipose tissue (VAT) accumulation. Here, we aimed to clarify the nature of this relationship and the underlying causality mechanism. METHODS: We conducted a population-based cross-sectional study comprising 8,504 subjects joining both NHANES 2003-2004 and 2011-2012 cycles and ENSANUT Medio Camino 2016. We performed mixed effects linear regression models using HOMA2-IR, adipoIR, and METS-VF as indicators of IR and VAT accumulation. Furthermore, we performed mediation analyses to assess a potential causal mechanism and ROC curves to establish cut-off points for identification of IR and visceral obesity using SUA. Finally, with an additional dataset comprised of 226 subjects with both euglycemic hyperinsulinemic clamp (EHC) and dual X-ray absorptiometry (DXA) measurements for IR and VAT accumulation, we performed a network of confirmatory mediation analyses. RESULTS:We found that SUA has a mediating role inside the bidirectional relationship between IR and visceral obesity, and it is part of an underlying causality mechanism which includes adiponectin. The proportion of the mechanism mediated by SUA is greater when stated that IR (in either peripheral or adipose tissue) leads to VAT accumulation (14.90%[13.20%-17.00%] and 15.54%[13.61% - 18.00%] to 4.88%[3.06%-7.00%] and 8.13%[5.91% - 10.00%]) instead of the opposite direction. This result was confirmed by mediation analyses using gold-standard measurements. CONCLUSIONS:Elevated SUA acts as mediator inside the bidirectional relationship between IR andVAT accumulation. Its role appears to be larger when considering adipose tissue IR as the promoter for VAT accumulation.

scholarly journals Protocatechuic acids protects against high glucose- induced insulin resistance in human visceral adipose tissue

2016 ◽  
Vol 62 (5) ◽  
pp. 45-46
Author(s):  
Paulina Ormazabal ◽  
Beatrice Scazzocchio ◽  
Rosaria Varì ◽  
Annunziata Iacovelli ◽  
Roberta Masella
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
High Glucose ◽  
Protective Role ◽  
Insulin Sensitizer ◽  
20 Nm ◽  
Visceral Adipose

Adipocytes exposed to high glucose concentrations exhibit impaired insulin signaling. Binding of insulin to its membrane receptor activates insulin metabolic pathway leading to IRS-1 and AKT phosphorylations. The accumulation of visceral adipose tissue (VAT) correlates with insulin resistance and metabolic syndrome. Anthocyanins (ACN) are bioactive food compounds of great nutritional interest. We have shown that protocatechuic acid (PCA), a major metabolite of ACN, might exert insulin-sensitizer activities in human visceral adipose tissue. The aim of this work was to define the protective role of PCA against insulin-resistance induced by high glucose in VAT.Methodology: VAT obtained from control subject (BMI≤25) were separated in four experimental groups: i) PCA: samples treated for 24 h with 100 μM PCA, ii) GLU: VAT treated with 30 mM glucose for 24 h, iii) PCA+GLU: 1 hour incubation with 100 μM PCA before adding glucose (30 mM, 24 h), iv) CTR: vehicle. After treatment, VAT groups were (or not) acutely stimulated with insulin (20 nM, 20 min). Tyr-IRS-1 and Ser-Akt phosphorylations were assessed by Western blotting (WB) in basal or insulin stimulated tissues in all experimental groups. Samples were assessed for IRS-1, IR, Akt and GLUT4 protein content by WB. Results: No differences in protein contents between experimental groups were found. GLU tissues showed a lower increment in insulin-stimulated phosphorylation of IRS-1 and Akt compared to CTR and PCA samples. This impaired activation was completely reversed by the pretreatment with PCA.Conclusion: An in-vitro insulin-resistance condition induced by high glucose was established in biopsies of VAT. PCA restores the ability of GLU-tissues to fully respond to insulin by increasing IRS-1 and Akt phosphorylations. These results confirm the insulin-sensitizer effect of PCA on VAT previously reported by our group. An anthocyanin rich diet might help to protect against insulin-resistance in VAT.

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