scholarly journals Obesity and Fat Metabolism in Human Immunodeficiency Virus–Infected Individuals: Immunopathogenic Mechanisms and Clinical Implications

2019 ◽  
Vol 220 (3) ◽  
pp. 420-431 ◽  
Author(s):  
Catherine Godfrey ◽  
Andrew Bremer ◽  
Diana Alba ◽  
Caroline Apovian ◽  
John R Koethe ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Adipose Tissue ◽  
Immune Cell ◽  
Clinical Care ◽  
Fat Metabolism ◽  
Visceral Obesity ◽  
Ectopic Fat ◽  
Metabolic Complications ◽  
Fat Accumulation ◽  
Immunodeficiency Virus

Abstract Metabolic complications relating to complex effects of viral and immune-mediated mechanisms are now a focus of clinical care among persons living with human immunodeficiency virus (PLHIV), and obesity is emerging as a critical problem. To address knowledge gaps, the US National Institutes of Health sponsored a symposium in May 2018 entitled “Obesity and Fat Metabolism in HIV-infected Individuals.” Mechanisms relating to adipose dysfunction and fibrosis, immune function, inflammation, and gastrointestinal integrity were highlighted as contributors to obesity among PLHIV. Fibrotic subcutaneous adipose tissue is metabolically dysfunctional and loses its capacity to expand, leading to fat redistribution, including visceral obesity and ectopic fat accumulation, promoting insulin resistance. Viral proteins, including viral protein R and negative regulatory factor, have effects on adipogenic pathways and cellular metabolism in resident macrophages and T cells. HIV also affects immune cell trafficking into the adipose compartments, with effects on adipogenesis, lipolysis, and ectopic fat accumulation. Key cellular metabolic functions are likely to be affected in PLHIV by gut-derived cytokines and altered microbiota. There are limited strategies to reduce obesity specifically in PLHIV. Enhancing our understanding of critical pathogenic mechanisms will enable the development of novel therapeutics that may normalize adipose tissue function and distribution, reduce inflammation, and improve insulin sensitivity in PLHIV.

scholarly journals Hypertrophic Obesity and Subcutaneous Adipose Tissue Dysfunction

2014 ◽  
Vol 6 (2) ◽  
pp. 79
Author(s):  
Anna Meiliana ◽  
Andi Wijaya
Keyword(s):  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Ectopic Fat ◽  
Metabolic Complications ◽  
Fat Accumulation ◽  
Insulin Resistant ◽  
Fat Redistribution ◽  
Subcutaneous Adipose

BACKGROUND: Over the past 50 years, scientists have recognized that not all adipose tissue is alike, and that health risk is associated with the location as well as the amount of body fat. Different depots are sufficiently distinct with respect to fatty-acid storage and release as to probably play unique roles in human physiology. Whether fat redistribution causes metabolic disease or whether it is a marker of underlying processes that are primarily responsible is an open question.CONTENT: The limited expandability of the subcutaneous adipose tissue leads to inappropriate adipose cell expansion (hypertrophic obesity) with local inflammation and a dysregulated and insulin-resistant adipose tissue. The inability to store excess fat in the subcutaneous adipose tissue is a likely key mechanism for promoting ectopic fat accumulation in tissues and areas where fat can be stored, including the intra-abdominal and visceral areas, in the liver, epi/pericardial area, around vessels, in the myocardium, and in the skeletal muscles. Many studies have implicated ectopic fat accumulation and the associated lipotoxicity as the major determinant of the metabolic complications of obesity driving systemic insulin resistance, inflammation, hepatic glucose production, and dyslipidemia.SUMMARY: In summary, hypertrophic obesity is due to an impaired ability to recruit and differentiate available adipose precursor cells in the subcutaneous adipose tissue. Thus, the subcutaneous adipose tissue may be particular in its limited ability in certain individuals to undergo adipogenesis during weight increase. Inability to promote subcutaneous adipogenesis under periods of affluence would favor lipid overlow and ectopic fat accumulation with negative metabolic consequences.KEYWORDS: obesity, adipogenesis, subcutaneous adipose tissue, visceral adipose tissue, adipocyte dysfunction

Relation of Subepicardial Adipose Tissue to Carotid Intima-Media Thickness in Patients With Human Immunodeficiency Virus

2007 ◽  
Vol 99 (10) ◽  
pp. 1470-1472 ◽  
Author(s):  
Gianluca Iacobellis ◽  
Adriano M. Pellicelli ◽  
Arya M. Sharma ◽  
Benvenuto Grisorio ◽  
Giorgio Barbarini ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Adipose Tissue ◽  
Intima Media Thickness ◽  
Carotid Intima Media Thickness ◽  
Media Thickness ◽  
Immunodeficiency Virus

scholarly journals Antiretroviral Therapy Initiation Is Associated With Decreased Visceral and Subcutaneous Adipose Tissue Density in People Living With Human Immunodeficiency Virus

2020 ◽  
Author(s):  
Paula Debroy ◽  
Jordan E Lake ◽  
Carlee Moser ◽  
Maxine Olefsky ◽  
Kristine M Erlandson ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Human Immunodeficiency Virus ◽  
Adipose Tissue ◽  
Antiretroviral Therapy ◽  
Hdl Cholesterol ◽  
Cd4 T Cell ◽  
Art Initiation ◽  
Immunodeficiency Virus ◽  
Hiv 1 ◽  
Cd4 T Cell Count

Abstract Background Adipose tissue (AT) alterations are common in people living with human immunodeficiency virus (PLWH). Decreases in AT density suggest disrupted adipocyte function/hypertrophy. We assessed changes in AT density after antiretroviral therapy (ART) initiation and associations with immunometabolic parameters. Methods In a prospective randomized clinical trial of ART initiation, L4–L5 abdominal CT scans measured subcutaneous AT (SAT) and visceral AT (VAT) area and density in treatment-naive PLWH randomized to tenofovir-emtricitabine plus ritonavir-boosted atazanavir, ritonavir-boosted darunavir, or raltegravir. Linear regression models compared week 0 and week 96 levels, and 96-week changes, in SAT and VAT density (in Hounsfield units [HU]). Spearman correlations assessed relationships between AT density and immunometabolic parameters. Results Of the 228 participants, 89% were male and 44% were white non-Hispanic. Median age was 36 years, baseline HIV-1 RNA was 4.6 log10 copies/mL, and CD4+ T-cell count was 344 cells/μL. Over 96 weeks, SAT and VAT HU decreased significantly in all arms. Less dense week 96 SAT and VAT density correlated with higher high-density lipoprotein (HDL) cholesterol and adiponectin (r = 0.19–0.30) levels and lower interleukin 6, non-HDL cholesterol, triglyceride, leptin, and homeostatic model assessment of insulin resistance (r = −0.23 to −0.68) levels at week 96 after adjusting for baseline CD4+ T-cell count, HIV-1 RNA, and baseline AT area. Conclusions Following virologic suppression, lower SAT and VAT density was associated with greater plasma measures of systemic inflammation, lipid disturbances, and insulin resistance independent of AT area, suggesting that changes in AT density with ART may lead to adverse health outcomes independent of AT quantity. Clinical Trials Registration NCT00851799.

Basal fuel homoeostasis in symptomatic human immunodeficiency virus infection

1991 ◽  
Vol 80 (4) ◽  
pp. 359-365 ◽  
Author(s):  
M. J. T. Hommes ◽  
J. A. Romijn ◽  
E. Endert ◽  
J. K. M. Eeftinck Schattenkerk ◽  
H. P. Sauerwein
Keyword(s):  
Human Immunodeficiency Virus ◽  
Fat Metabolism ◽  
Glucose Turnover ◽  
Short Term ◽  
Control Subjects ◽  
Immunodeficiency Virus ◽  
Healthy Control ◽  
Overnight Fasting ◽  
And Control ◽  
Symptomatic Human Immunodeficiency Virus

1. In eight clinically stable symptomatic human-immunodeficiency-virus-infected patients and in seven healthy control subjects, glucose and fat metabolism were studied, using indirect calorimetry and primed continuous infusions of [3-3H]glucose and [14C]palmitate. 2. Studies were performed in the post-absorptive state (16 h of overnight fasting) and again after 22 h of overnight fasting. 3. In the post-absorptive state, net fat oxidation and triacylglycerol (‘triglyceride’) concentrations were significantly higher in the patients, but concentrations and turnover of free fatty acids were not significantly different between patients and control subjects. After 22 h of overnight fasting, free fatty acid turnover in the patients rose to significantly higher levels when compared with the control subjects. 4. Post-absorptive glucose oxidation, glucose turnover and glucose clearance did not differ between patients and control subjects. Although fasting induced a significantly greater decline in glucose turnover in the patients, plasma glucose concentrations decreased comparably in patients and control subjects. 5. No differences were found in plasma concentrations of insulin or of the counter-regulatory hormones between patients and control subjects. 6. It is concluded that the metabolic adaptation to short-term starvation in clinically stable human-immunodeficiency-virus-infected patients differs from that in healthy control subjects. Short-term starvation results in a significantly greater fall in glucose turnover, whereas fat metabolism is clearly stimulated. These alterations cannot be explained by differences in the concentrations of insulin or of the counter-regulatory hormones.

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