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Association between Subcutaneous Adipose Tissue Inflammation, Insulin Resistance, and Calorie Restriction in Obese Females.
Sbierski-Kind, J, Mai, K, Kath, J, Jurisch, A, Streitz, M, Kuchenbecker, L, Babel, N, Nienen, M, Jürchott, K, Spranger, L, et al
Journal of immunology (Baltimore, Md. : 1950). 2020;(1):45-55
Abstract
The worldwide epidemic of overweight and obesity has led to an increase in associated metabolic comorbidities. Obesity induces chronic low-grade inflammation in white adipose tissue (WAT). However, the function and regulation of both innate and adaptive immune cells in human WAT under conditions of obesity and calorie restriction (CR) is not fully understood yet. Using a randomized interventional design, we investigated postmenopausal overweight or obese female subjects who either underwent CR for 3 mo followed by a 4-wk phase of weight maintenance or had to maintain a stable weight over the whole study period. A comprehensive immune phenotyping protocol was conducted using validated multiparameter flow cytometry analysis in blood and s.c. WAT (SAT). The TCR repertoire was analyzed by next-generation sequencing and cytokine levels were determined in SAT. Metabolic parameters were determined by hyperinsulinemic-euglycemic clamp. We found that insulin resistance correlates significantly with a shift toward the memory T cell compartment in SAT. TCR analysis revealed a diverse repertoire in SAT of overweight or obese individuals. Additionally, whereas weight loss improved systemic insulin sensitivity in the intervention group, SAT displayed no significant improvement of inflammatory parameters (cytokine levels and leukocyte subpopulations) compared with the control group. Our data demonstrate the accumulation of effector memory T cells in obese SAT and an association between systemic glucose homeostasis and inflammatory parameters in obese females. The long-standing effect of obesity-induced changes in SAT was demonstrated by preserved immune cell composition after short-term CR-induced weight loss.
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Microbes: possible link between modern lifestyle transition and the rise of metabolic syndrome.
Moossavi, S, Bishehsari, F
Obesity reviews : an official journal of the International Association for the Study of Obesity. 2019;(3):407-419
Abstract
The rapid decrease in infectious diseases globally has coincided with an increase in the prevalence of obesity and other components of metabolic syndrome. Insulin resistance is a common feature of metabolic syndrome and can be influenced by genetic and non-genetic/environmental factors. The emergence of metabolic syndrome epidemics over only a few decades suggests a more prominent role of the latter. Changes in our environment and lifestyle have indeed paralleled the rise in metabolic syndrome. Gastrointestinal tract microbiota, the composition of which plays a significant role in host physiology, including metabolism and energy homeostasis, are distinctly different within the context of metabolic syndrome. Among humans, recent lifestyle-related changes could be linked to changes in diversity and composition of 'ancient' microbiota. Given the co-adaptation and co-evolution of microbiota with the immune system over a long period of time, it is plausible that such lifestyle-related microbiota changes could trigger aberrant immune responses, thereby predisposing an individual to a variety of diseases. Here, we review current evidence supporting a role for gut microbiota in the ongoing rise of metabolic syndrome. We conclude that population-level shifts in microbiota can play a mediatory role between lifestyle factors and pathogenesis of insulin resistance and metabolic syndrome.
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Association of Gut Intestinal Integrity and Inflammation with Insulin Resistance in Adults Living with HIV in Uganda.
Reid, MJA, Ma, Y, Golovaty, I, Okello, S, Sentongo, R, Feng, M, Tsai, AC, Kakuhikire, B, Tracy, R, Hunt, PW, et al
AIDS patient care and STDs. 2019;(7):299-307
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Abstract
We conducted a cross-sectional study of 148 HIV+ on HIV antiretroviral therapy and 149 HIV- adults in Mbarara, Uganda, to estimate the association between HIV infection and homeostasis model assessment of insulin resistance (HOMA-IR) using multivariable regression analysis. In addition, we evaluated whether intestinal fatty acid-binding protein (I-FABP), monocyte activation markers soluble (s)CD14 and sCD163, and proinflammatory cytokine interleukin 6 (IL-6) mediated this association. HOMA-IR was greater among HIV+ than HIV- adults [median (interquartile range): 1.3 (0.7-2.5) vs. 0.9 (0.5-2.4); p = 0.008]. In models adjusted for sociodemographic variables, diet, hypertension, and smoking history, HIV infection was associated with 37% [95% confidence intervals (95% CIs): 5-77] greater HOMA-IR compared with HIV- participants. The magnitude of association was greater when I-FABP was included as a covariate although the additive effect was modest (40% CI: 8-82). By contrast adding sCD14 to the model was associated with greater HOMA-IR (59%; 95% CI: 21-109) among HIV+ participants compared with HIV- participants. Among HIV+ participants, greater CD4 nadir was non-significantly associated with greater HOMA-IR (22%; 95% CI: -2 to 52). Each 5-unit increase in body mass index (BMI; 49% greater HOMA-IR; 95% CI: 18-87) and female sex (71%; 95% CI: 17-150) remained associated in adjusted models. In this study of mainly normal-weight Ugandan adults, HIV infection, female sex, and greater BMI were all associated with greater insulin resistance (IR). This association was strengthened modestly after adjustment for sCD14, suggesting possible distinct immune pathways to IR that are independent of HIV or related to inflammatory changes occurring on HIV treatment.
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Interplay between the Adaptive Immune System and Insulin Resistance in Weight Loss Induced by Bariatric Surgery.
Villarreal-Calderón, JR, Cuéllar, RX, Ramos-González, MR, Rubio-Infante, N, Castillo, EC, Elizondo-Montemayor, L, García-Rivas, G
Oxidative medicine and cellular longevity. 2019;:3940739
Abstract
Low-grade chronic inflammation plays a pivotal role among other pathophysiological mechanisms involved in obesity. Innate and adaptive immune cells undergo systemic proinflammatory polarization that gives rise to an increased secretion of proinflammatory cytokines, which in turn leads to insulin resistance. Bariatric surgery is currently the most effective treatment for obesity, as it brings on significant weight loss, glucose metabolism improvement, and a decrease in systemic inflammation biomarkers. After bariatric surgery, several changes have been reported to occur in adaptive immunity, including reduction in CD4+ and CD8+ T cell counts, a decrease in the Th1/Th2 ratio, an increase in B regulatory cells, and reduction in proinflammatory cytokine secretion. Overall, there seems to be a major shift in several lymphocyte populations from a proinflammatory to an anti-inflammatory phenotype. Furthermore, increased antioxidant activity and reduced lipid and DNA oxidation products have been reported after bariatric surgery in circulating mononuclear cells. This paper highlights the shift in the adaptive immune system in response to weight loss and improved insulin sensitivity, as well as the interplay between immunological and metabolic adaptations as a result of bariatric surgery. Finally, based on data from research, we propose several mechanisms such as changes in adaptive immune cell phenotypes and their by-products, recruitment in adipose tissue, reduced oxidative stress, and modification in metabolic substrate availability as drivers to reduce low-grade chronic inflammation after bariatric surgery in severe obesity.
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Association Between Cortisol, Insulin Resistance and Zinc in Obesity: a Mini-Review.
Morais, JBS, Severo, JS, Beserra, JB, de Oiveira, ARS, Cruz, KJC, de Sousa Melo, SR, do Nascimento, GVR, de Macedo, GFS, do Nascimento Marreiro, D
Biological trace element research. 2019;(2):323-330
Abstract
Adipose tissue is considered an endocrine organ and its excess compromises the immune response and the metabolism of hormones and nutrients. Furthermore, visceral fat accumulation contributes to increased cortisol synthesis, which in turn induces metallothionein and Zip14 expression, which are proteins that contribute to reducing plasma zinc levels. Zinc plays a critical role in the secretion and signaling of insulin. Changes in the biochemical parameters of zinc, as observed in individuals who are obese, contribute to the manifestation of related disorders such as insulin resistance. Thus, the purpose of this review is to provide an update on the current information on the relationship between cortisol, zinc, and insulin resistance in obesity. The data in the literature provide evidence that cortisol affects zinc metabolism, and indicate possible repercussions on insulin signaling that might contribute to the development of resistance to the actions of insulin in obesity.
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Insulin resistance - "the good or the bad and ugly".
Szosland, K, Lewinski, A
Neuro endocrinology letters. 2018;(5):355-362
Abstract
Insulin resistance (IR) is a state of decreased sensitivity or responsiveness of target tissues to metabolic actions of circulating insulin. IR can be selective, involving only certain aspects of insulin action, i.e. only its impact on hepatic glucose disposal. Plasma insulin concentration is a continuous variable, dependent upon several physiological stimuli, thus the thresholds used to diagnose IR are arbitrary. Insulin resistance (impaired insulin action) may occur due to derangements on three levels: pre-receptor (antibodies against insulin, defected insulin molecule), receptor (defects of insulin receptor, anti-receptor antibodies) and post-receptor (disregulated intracellular pathways). The aim of the study has been promoting the opinion that IR itself cannot be considered only a harmful phenomenon. Detrimental effect is rather chronic hyperinsulinemia related to IR. IR appears important physiological mechanism responsible for adaptation to various stresses: physical, as well as emotional/physiological. Diurnal, seasonal, age-related, pregnancy-associated, and illness-induced fluctuations in food intake and energy expenditure necessitate homeostatic versatility, including the capacity to vary insulin sensitivity, so as to optimize partitioning between tissues of a variable nutrient supply. IR has positively been selected during evolution for the short-lived energy-consuming activation of the brain or immune system. Physiologic situations that require organisms to reserve priority nutrient access for an emerging metabolic requirement, for example immune system activation or foetal development, promote the decrease of systemic insulin sensitivity, reducing nutrient uptake by non-priority tissues and reserving glucose for priority cells. It has been suggested that IR is a mechanism of antioxidant defence in conditions of nutrient energy excess.