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1.
Prehabilitation: metabolic considerations.
Chabot, K, Gillis, C, Carli, F
Current opinion in clinical nutrition and metabolic care. 2020;(4):271-276
Abstract
PURPOSE OF REVIEW The major components of ERAS attenuate the inflammatory response and modulate metabolism in direction of sparing body protein and preserving function. However, these perioperative interventions might have limited effectiveness on postoperative outcomes if preoperative risk factors are not addressed and optimized. RECENT FINDINGS The preoperative metabolic perturbations characterized by insulin resistance and sarcopenia might predispose patients to a higher degree of postoperative catabolism. High-risk populations for such metabolic disturbances include elderly and frail patients, and patients with metabolic syndrome. Research on the effect of prehabilitation on perioperative metabolism is limited, but recent findings suggest that interventions designed to improve insulin sensitivity prior to surgery might represent a promising therapeutic target to minimize surgical complications. SUMMARY The present paper will discuss the metabolic implications of modulating preoperative risk factors with elements of multimodal prehabilitation, such as exercise training and nutrition.
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2.
Hypoxia and exercise interactions on skeletal muscle insulin sensitivity in obese subjects with metabolic syndrome: results of a randomized controlled trial.
Mai, K, Klug, L, Rakova, N, Piper, SK, Mähler, A, Bobbert, T, Schulz-Menger, J, Spranger, J, Boschmann, M, Luft, FC
International journal of obesity (2005). 2020;(5):1119-1128
Abstract
BACKGROUND Physical activity improves insulin sensitivity in obesity. Hypoxia training is claimed to augment this effect. We tested the hypothesis that normobaric hypoxia training would improve insulin sensitivity in obese patients with metabolic syndrome. METHODS In a randomized controlled trial, 23 obese men with metabolic syndrome who were not informed of the FiO2 conditions underwent a 6-week physical exercise intervention under ambient (n = 11; FiO2 21%) conditions or hypoxia (n = 12; FiO2 15%) using a normobaric hypoxic chamber. Three 60-min sessions of interval training were performed each week at 60% of individual V̇O2max. Assessment of myocellular insulin sensitivity by euglycemic hyperinsulinemic clamp was performed in 21 of these subjects before and after 6 weeks of training. Comprehensive phenotyping also included biopsies of subcutaneous adipose tissues. RESULTS The intermittent moderate physical exercise protocol did not substantially change the myocellular insulin sensitivity within 6 weeks under normoxic conditions (ISIClamp: 0.035 (IQR 0.016-0.075) vs. 0.037 (IQR 0.026-0.056) mg* kg-1 *min-1/(mU* l-1); p = 0.767). In contrast, ISIClamp improved during hypoxia training (0.028 (IQR 0.018-0.035) vs. 0.038 (IQR 0.024-0.060) mg * kg-1 *min-1/(mU *l-1); p < 0.05). Between group comparison of ISIClamp change revealed a small difference between groups (Cohen's d = 0.26). Within the hypoxic group, improvement of ISIClamp during training was associated with individual increase of circulating vascular endothelial growth factor (VEGF) levels (r = 0.678, p = 0.015), even if mean VEGF levels were not modified by any training condition. Atrial natriuretic peptide (ANP) system components were not associated with increased ISIClamp during hypoxic training. CONCLUSIONS Physical training under hypoxic conditions could partially augment the favorable effects of exercise alone on myocellular insulin sensitivity in obese men with metabolic syndrome. Concomitant changes in VEGF might represent an underlying pathophysiological mechanism.
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3.
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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4.
Indirect insulin resistance detection: Current clinical trends and laboratory limitations.
Placzkowska, S, Pawlik-Sobecka, L, Kokot, I, Piwowar, A
Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia. 2019;(3):187-199
Abstract
There is a steady increase in the number of overweight and obese people worldwide and increasingly, younger people. Excess adipose tissue impairs the action of insulin, leading to insulin resistance (IR). Tissue IR is a major factor in relation to cardiovascular disease, metabolic syndrome and diabetes. Thus, it is important to recognize at the pre-disease stage with the possibility of therapeutic intervention. IR is assessed using indicators of epidemiological significance, most often calculated from fasting and postprandial glucose and insulin values, so-called indirect indicators of insulin resistance. The most commonly used parameter is the Homeostatic Model Assessment (HOMA). Although the Quantitative Insulin Sensitivity Check Index (QUICKI), Matsuda Index and the Insulin Secretion-Sensitivity Index-2 (ISSI-2) are also used, the values of these indices established for IR vary for different age, sex, populations and ethnic groups. Thus, appropriate reference values of indirect indices should be determined for such groups, and when this is precluded, data from published studies carried out on the most ethnically, socio-economically and age-matched populations should be applied.
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5.
High HOMA-IR Index in Healthcare Shift Workers.
Ledda, C, Cinà, D, Matera, S, Mucci, N, Bracci, M, Rapisarda, V
Medicina (Kaunas, Lithuania). 2019;(5)
Abstract
Background and objectives: Evidence shows that shift work may be correlated with insulin resistance (IR). Therefore its estimation in clinical and prevention practice is of great significance. A cross-sectional study was performed to examine the Homeostasis Model Assessment-Insulin Resistance (HOMA-IR) Index among healthcare shift workers (HCSW). Materials and Methods: A total of 272 healthcare workers (HCWs) were invited to participate in the study within an occupational surveillance framework, 137 were HCSW while 135 were healthcare non-shift workers (HCNSW). Fasting glucose, insulin, and HOMA-IR Index were evaluated in each participant and correlated with shift workers. Results: Indicators of glucose metabolism were significantly higher in HCSW p < 0.001, and logistic regression analysis confirmed a significant positive association between increased values of HOMA-IR Index and shift workers (p < 0.05). Conclusions: Shift work could be a risk factor in developing insulin resistance and metabolic syndrome.
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Fine-scale haplotype mapping of MUT, AACS, SLC6A15 and PRKCA genes indicates association with insulin resistance of metabolic syndrome and relationship with branched chain amino acid metabolism or regulation.
Haydar, S, Grigorescu, F, Vintilă, M, Cogne, Y, Lautier, C, Tutuncu, Y, Brun, JF, Robine, JM, Pugeat, M, Normand, C, et al
PloS one. 2019;(3):e0214122
Abstract
Branched chain amino acids (BCAA) are essential elements of the human diet, which display increased plasma levels in obesity and regained particular interest as potential biomarkers for development of diabetes. To define determinants of insulin resistance (IR) we investigated 73 genes involved in BCAA metabolism or regulation by fine-scale haplotype mapping in two European populations with metabolic syndrome. French and Romanians (n = 465) were genotyped for SNPs (Affymetrix) and enriched by imputation (BEAGLE 4.1) at 1000 genome project density. Initial association hits detected by sliding window were refined (HAPLOVIEW 3.1 and PHASE 2.1) and correlated to homeostasis model assessment (HOMAIR) index, in vivo insulin sensitivity (SI) and BCAA plasma levels (ANOVA). Four genomic regions were associated with IR located downstream of MUT, AACS, SLC6A15 and PRKCA genes (P between 9.3 and 3.7 x 10-5). Inferred haplotypes up to 13 SNPs length were associated with IR (e.g. MUT gene with P < 4.9 x 10-5; Bonferroni 1.3 x 10-3) and synergistic to HOMAIR. SNPs in the same regions were also associated with one order of magnitude lower P values (e.g. rs20167284 in the MUT gene with P < 1.27 x 10-4) and replicated in Mediterranean samples (n = 832). In French, influential haplotypes (OR > 2.0) were correlated with in vivo insulin sensitivity (1/SI) except for SLC6A15 gene. Association of these genes with BCAA levels was variable, but influential haplotypes confirmed implication of MUT from BCAA metabolism as well as a role of regulatory genes (AACS and PRKCA) and suggested potential changes in transcriptional activity. These data drive attention towards new regulatory regions involved in IR in relation with BCAA and show the ability of haplotypes in phased DNA to detect signals complimentary to SNPs, which may be useful in designing genetic markers for clinical applications in ethnic populations.
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7.
Endocrinopathies and cancer cachexia.
Dev, R, Del Fabbro, E, Dalal, S
Current opinion in supportive and palliative care. 2019;(4):286-291
Abstract
PURPOSE OF REVIEW Cancer cachexia cannot be easily reversed by standard nutritional support and interventions directed at underlying metabolic derangements may be needed to prevent or reverse cachexia and maintain healthy body composition. The following review will highlight the contribution and potential therapeutic interventions for insulin resistance, alterations in ghrelin signaling, and hypogonadism in cancer patients. RECENT FINDINGS In addition to decreased caloric intake, chronic inflammation, and altered metabolism of glucose, proteins and lipids, endocrine abnormalities can propagate weight loss or changes in body composition in cancer patients. SUMMARY Cancer cachexia, loss of muscle mass with or without the loss of fat mass, is a multifactorial syndrome, which is associated with increased morbidity and mortality. Currently, limited therapeutic options for the treatment of weight loss in cancer patients exist, which lead to clinically meaningful improvements in weight gain and performance status. Treatment directed at underlying insulin resistance, low testosterone, and altered ghrelin sensitivity, in the future, may lead to potential therapeutic options for loss of lean body mass and cancer cachexia.
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A randomized control trial of the impact of LCPUFA-ω3 supplementation on body weight and insulin resistance in pubertal children with obesity.
López-Alarcón, M, Inda-Icaza, P, Márquez-Maldonado, MC, Armenta-Álvarez, A, Barbosa-Cortés, L, Maldonado-Hernández, J, Piña-Aguero, M, Barradas-Vázquez, A, Núñez-García, BA, Rodríguez-Cruz, M, et al
Pediatric obesity. 2019;(5):e12499
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Abstract
BACKGROUND Paediatric obesity and insulin resistance (IR) are potentially reversible inflammatory conditions. Long chain polyunsaturated fatty acids omega-3 (LCPUFA-ω3) show anti-inflammatory and metabolic properties, but their clinical efficacy is unclear. OBJECTIVE The objective of this study is to evaluate whether supplementation with LCPUFA-ω3 for 3 months reduces insulin resistance and weight to adolescents with obesity. METHODS Double-blind trial of 366 adolescents with obesity randomly assigned to 1.2-g LCPUFA-ω3 (DO3) or 1-g sunflower oil (DP) daily for 3 months; both groups received an energy-restricted diet. Children attended monthly for anthropometric, dietary, and clinical measurements. Basal and final blood samples were obtained to measure metabolic markers and erythrocytes fatty acids. Regression models were used for analysis. RESULTS A total of 119 DO3 and 126 DP children completed follow-up. At baseline, 92% of children presented IR, 66% hypertriglyceridemia, 37% low-grade inflammation, and 32% metabolic syndrome. Despite erythrocytes LCPUFA-ω3 increased more in DO3 (Median differences = 0.984 w/w%; 95 IC = 0.47, 1.53, P < 0.001), body weight, insulin, and HOMA changed similarly in both groups at the end of intervention. Adjusting for basal values, changes in weight, insulin, and HOMA was not related with supplementation. CONCLUSIONS Supplementation with LCPUFA-ω3 does not affect body weight or insulin in adolescents with obesity.
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The Effect of Low Glycemic Index and Glycemic Load Diets on Hepatic Fat Mass, Insulin Resistance, and Blood Lipid Panels in Individuals with Nonalcoholic Fatty Liver Disease.
Parker, A, Kim, Y
Metabolic syndrome and related disorders. 2019;(8):389-396
Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease that is associated with insulin resistance and hepatic triglyceride accumulation. There is evidence to suggest that a low glycemic index (GI) diet can reduce glucose absorption, hepatic influx of glucose, and de novo lipogenesis. This review investigates the effect of low GI and glycemic load (GL) diets on hepatic fat mass, hepatic enzymes, insulin resistance, fasting blood glucose levels, and blood lipid panels in individuals with NAFLD. PubMed, Cumulative Index to Nursing and Allied Health Literature, and Web of Science were used in literature search. Search keywords included "glycemic index," "glycaemic index," "glycemic load," "glycaemic load," "nonalcoholic fatty liver disease," "NAFLD," "nonalcoholic steatohepatitis," and "NASH." Outcome measurements included hepatic fat mass, hepatic enzyme alanine transaminase (ALT), insulin resistance [homeostasis model assessment of insulin resistance (HOMA-IR)], fasting blood glucose levels, and/or blood lipid panels. Four eligible studies enrolling 281 individuals with NAFLD were included. Both hepatic fat mass and ALT showed significant reductions from baseline in both low GI and GL diets. One study showed no change, and another study showed significant reductions in HOMA-IR. No significant reduction in fasting blood glucose level, triglycerides, high-density lipoprotein-cholesterol, or low-density lipoprotein-cholesterol was observed from baseline in both low GI and GL diets. Findings from the review suggest that low GI and GL diets may reduce hepatic fat mass and ALT in individuals with NAFLD. Future research of large-scale, randomized controlled studies using isoenergetic, low GI and GL diets for long term is needed to draw conclusionary results.
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Metabolic syndrome in polycystic ovary syndrome: a systematic review, meta-analysis and meta-regression.
Lim, SS, Kakoly, NS, Tan, JWJ, Fitzgerald, G, Bahri Khomami, M, Joham, AE, Cooray, SD, Misso, ML, Norman, RJ, Harrison, CL, et al
Obesity reviews : an official journal of the International Association for the Study of Obesity. 2019;(2):339-352
Abstract
Women with polycystic ovary syndrome (PCOS) have increased risk of metabolic syndrome. The relative contribution of clinical, demographic or biochemical factors to metabolic syndrome in PCOS is not known. A literature search was conducted in MEDLINE, CINAHL, EMBASE and clinical trial registries. Of 4530 studies reviewed, 59 were included in the systematic review and 27 in the meta-analysis and meta-regression. In good and fair quality studies, women with PCOS had an overall increased prevalence of metabolic syndrome (odds ratio, OR 3.35, 95% confidence interval, CI 2.44, 4.59). Increased prevalence of metabolic syndrome occurred in overweight or obese women with PCOS (OR 1.88, 95% 1.16, 3.04) but not in lean women (OR 1.45, 95% CI 0.35, 6.12). In meta-regression analyses, the markers of metabolic syndrome diagnostic criteria (waist circumference, high-density lipoprotein cholesterol, triglyceride, blood pressure), BMI, glucose tolerance (2-hr oral glucose tolerance test) and surrogate markers of insulin resistance (HOMA-IR) but not markers of reproductive dysfunction (sex hormone binding globulin, testosterone, PCOS phenotypes) contributed significantly to the heterogeneity in the prevalence of metabolic syndrome. Women with PCOS have increased risk of metabolic syndrome which was associated with obesity and metabolic features but not with indices of hyperandrogenism.