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Abdominal and gluteofemoral fat depots show opposing associations with postprandial lipemia.
Christiansen, MR, Ureña, MG, Borisevich, D, Grarup, N, Martínez, JA, Oppert, JM, Sørensen, TI, Hansen, T, Blaak, EE, Kilpeläinen, TO
The American journal of clinical nutrition. 2021;(4):1467-1475
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Abstract
BACKGROUND High postprandial lipemia is associated with increased risk of cardiovascular disease, independently of fasting lipid concentrations. Abdominal and gluteofemoral fat depots handle lipoproteins differently, which could affect postprandial lipemia and contribute to the relation between abdominal fat distribution and cardiovascular disease risk. OBJECTIVES We aimed to study the influences of higher abdominal compared with gluteofemoral fat on postprandial lipemia after a high-fat meal in individuals with obesity. METHODS A total of 755 adults with obesity from a randomized controlled trial in 7 European countries consumed a liquid high-fat meal. Concentrations of triglycerides (TG), glycerol, free fatty acids, and the cholesterol component of remnant-like particles (RLP), LDL, and HDL were measured postprandially for 3 h. Associations of waist circumference (WC), hip circumference (HC), and waist-hip ratio (WHR) with changes in postprandial lipid concentrations, adjusted for fasting concentrations and BMI, were examined using linear regression models. To assess whether the association of WHR with postprandial lipemia could be causal, we performed instrumental variable analyses using a genetic score of 442 variants known to be associated with WHR adjusted for BMI in 2-stage least-squares regression models. RESULTS WHR was associated with higher TG and RLP cholesterol concentrations, independent of fasting lipid concentrations and BMI. Instrumental variable analyses suggested that the associations of WHR with postprandial TG (β = 0.038 μmol/L*min, SE = 0.019 μmol/L*min, P = 0.044) and RLP cholesterol concentrations (β = 0.059 mmol/L, SE = 0.025 mmol/L, P = 0.020) may be causal. WC and HC showed opposite effects: higher WC was associated with higher TG and RLP cholesterol concentrations whereas higher HC was associated with lower concentrations. CONCLUSIONS Our results suggest that higher fat deposition abdominally versus gluteofemorally may be causally associated with elevated postprandial lipemia after a high-fat meal, independent of fasting lipid concentrations and BMI. Furthermore, higher abdominal and gluteofemoral fat depots show opposing effects on postprandial lipemia.This trial was registered at www.isrctn.com as ISRCTN25867281.
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Increased postprandial nonesterified fatty acid efflux from adipose tissue in prediabetes is offset by enhanced dietary fatty acid adipose trapping.
Montastier, É, Ye, RZ, Noll, C, Bouffard, L, Fortin, M, Frisch, F, Phoenix, S, Guérin, B, Turcotte, ÉE, Lewis, GF, et al
American journal of physiology. Endocrinology and metabolism. 2021;(6):E1093-E1106
Abstract
The mechanism of increased postprandial nonesterified fatty acid (NEFA) appearance in the circulation in impaired glucose tolerance (IGT) is due to increased adipose tissue lipolysis but could also be contributed to by reduced adipose tissue (AT) dietary fatty acid (DFA) trapping and increased "spillover" into the circulation. Thirty-one subjects with IGT (14 women, 17 men) and 29 with normal glucose tolerance (NGT, 15 women, 14 men) underwent a meal test with oral and intravenous palmitate tracers and the oral [18F]-fluoro-thia-heptadecanoic acid positron emission tomography method. Postprandial palmitate appearance (Rapalmitate) was higher in IGT versus NGT (P < 0.001), driven exclusively by Rapalmitate from obesity-associated increase in intracellular lipolysis (P = 0.01), as Rapalmitate from DFA spillover was not different between the groups (P = 0.19) and visceral AT DFA trapping was even higher in IGT versus NGT (P = 0.02). Plasma glycerol appearance was lower in IGT (P = 0.01), driven down by insulin resistance and increased insulin secretion. Thus, we found higher AT DFA trapping, limiting spillover to lean organs and in part offsetting the increase in Rapalmitate from intracellular lipolysis. Whether similar findings occur in frank diabetes, a condition also characterized by insulin resistance but relative insulin deficiency, requires further investigation (Clinicaltrials.gov: NCT04088344, NCT02808182).NEW & NOTEWORTHY We found higher adipose tissue dietary fatty acid trapping, limiting spillover to lean organs, that in part offsets the increase in appearance rate of palmitate from intracellular lipolysis in prediabetes. These results point to the adaptive nature of adipose tissue trapping and dietary fatty acid spillover as a protective mechanism against excess obesity-related palmitate appearance rate from intracellular adipose tissue lipolysis.
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Fetuin-B, a potential link of liver-adipose tissue cross talk during diet-induced weight loss-weight maintenance.
Li, L, Spranger, L, Stobäus, N, Beer, F, Decker, AM, Wernicke, C, Brachs, S, Brachs, M, Spranger, J, Mai, K
Nutrition & diabetes. 2021;(1):31
Abstract
BACKGROUND/OBJECTIVES Numerous hepatokines are involved in inter-organ cross talk regulating tissue-specific insulin sensitivity. Adipose tissue lipolysis represents a crucial element of adipose insulin sensitivity and is substantially involved in long-term body weight regulation after dietary weight loss. Thus, we aimed to analyze the impact of the hepatokine Fetuin-B in the context of weight loss induced short- and long-term modulation of adipose insulin sensitivity. SUBJECTS/METHODS 143 subjects (age > 18; BMI ≥ 27 kg/m2) were analyzed before (T-3) and after (T0) a standardized 12-week dietary weight reduction program. Afterward, subjects were randomized to a 12-month lifestyle intervention or a control group. After 12 months (T12) no further intervention was performed until 6 months later (T18) (Maintain-Adults trial). Tissue-specific insulin sensitivity was estimated by HOMA-IR (predominantly liver), ISIClamp (predominantly skeletal muscle), and free fatty acid suppression during hyperinsulinemic-euglycemic clamp (FFASupp) (predominantly adipose tissue). Fetuin-B was measured at all concomitant time points. RESULTS Circulating Fetuin-B levels correlated significantly with estimates of obesity, hepatic steatosis as well as HOMA-IR, ISIClamp, FFASupp at baseline. Fetuin-B decreased during dietary weight loss (4.2 (3.5-4.9) vs. 3.8 (3.2-4.6) µg/ml; p = 2.1 × 10-5). This change was associated with concomitant improvement of HOMA-IR (r = 0.222; p = 0.008) and FFASupp (r = -0.210; p = 0.013), suggesting a particular relationship to hepatic and adipose tissue insulin sensitivity. Weight loss induced improvements of insulin resistance were almost completely preserved until months 12 and 18 and most interestingly, the short and long-term improvement of FFASupp was partially predicted by baseline level of Fetuin-B. CONCLUSIONS Our data suggest that Fetuin-B might be a potential mediator of liver-adipose cross talk involved in short- and long-term regulation of adipose insulin sensitivity, especially in the context of diet-induced weight changes. TRIAL REGISTRATION ClinicalTrials.gov number: NCT00850629, https://clinicaltrials.gov/ct2/show/NCT00850629 , date of registration: February 25, 2009.
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Inter-Day Reliability of Resting Metabolic Rate and Maximal Fat Oxidation during Exercise in Healthy Men Using the Ergostik Gas Analyzer.
Robles-González, L, Gutiérrez-Hellín, J, Aguilar-Navarro, M, Ruiz-Moreno, C, Muñoz, A, Del-Coso, J, R Ruiz, J, Amaro-Gahete, FJ
Nutrients. 2021;(12)
Abstract
The attainment of high inter-day reliability is crucial to determine changes in resting metabolic rate (RMR), respiratory exchange ratio (RER), maximal fat oxidation during exercise (MFO) and the intensity that elicits MFO (Fatmax) after an intervention. This study aimed to analyze the inter-day reliability of RMR, RER, MFO and Fatmax in healthy adults using the Ergostik gas analyzer. Fourteen healthy men (age: 24.4 ± 5.0 years, maximum oxygen uptake (VO2max): 47.5 ± 11.9 mL/kg/min) participated in a repeated-measures study. The study consisted of two identical experimental trials (Day 1 and Day 2) in which the participants underwent an indirect calorimetry assessment at resting and during an incremental exercise test. Stoichiometric equations were used to calculate energy expenditure and substrate oxidation rates. There were no significant differences when comparing RMR (1999.3 ± 273.9 vs. 1955.7 ± 362.6 kcal/day, p = 0.389), RER (0.87 ± 0.05 vs. 0.89 ± 0.05, p = 0.143), MFO (0.32 ± 0.20 vs. 0.31 ± 0.20 g/min, p = 0.776) and Fatmax (45.0 ± 8.6 vs. 46.4 ± 8.4% VO2max, p = 0.435) values in Day 1 vs. Day 2. The inter-day coefficient of variation for RMR, RER, MFO and Fatmax were 4.85 ± 5.48%, 3.22 ± 3.14%, 7.78 ± 5.51%, and 6.51 ± 8.04%, respectively. In summary, the current results show a good inter-day reliability when RMR, RER, MFO and Fatmax are determined in healthy men using the Ergostik gas analyzer.
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Achieving an Optimal Fat Loss Phase in Resistance-Trained Athletes: A Narrative Review.
Ruiz-Castellano, C, Espinar, S, Contreras, C, Mata, F, Aragon, AA, Martínez-Sanz, JM
Nutrients. 2021;(9)
Abstract
Managing the body composition of athletes is a common practice in the field of sports nutrition. The loss of body weight (BW) in resistance-trained athletes is mainly conducted for aesthetic reasons (bodybuilding) or performance (powerlifting or weightlifting). The aim of this review is to provide dietary-nutritional strategies for the loss of fat mass in resistance-trained athletes. During the weight loss phase, the goal is to reduce the fat mass by maximizing the retention of fat-free mass. In this narrative review, the scientific literature is evaluated, and dietary-nutritional and supplementation recommendations for the weight loss phase of resistance-trained athletes are provided. Caloric intake should be set based on a target BW loss of 0.5-1.0%/week to maximize fat-free mass retention. Protein intake (2.2-3.0 g/kgBW/day) should be distributed throughout the day (3-6 meals), ensuring in each meal an adequate amount of protein (0.40-0.55 g/kgBW/meal) and including a meal within 2-3 h before and after training. Carbohydrate intake should be adapted to the level of activity of the athlete in order to training performance (2-5 g/kgBW/day). Caffeine (3-6 mg/kgBW/day) and creatine monohydrate (3-5 g/day) could be incorporated into the athlete's diet due to their ergogenic effects in relation to resistance training. The intake of micronutrients complexes should be limited to special situations in which there is a real deficiency, and the athlete cannot consume through their diet.
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Placebo Effect of Caffeine on Substrate Oxidation during Exercise.
Gutiérrez-Hellín, J, Ruiz-Moreno, C, Aguilar-Navarro, M, Muñoz, A, Varillas-Delgado, D, Amaro-Gahete, FJ, Roberts, JD, Del Coso, J
Nutrients. 2021;(3)
Abstract
By using deceptive experiments in which participants are informed that they received caffeine when, in fact, they received an inert substance (i.e., placebo), several investigations have demonstrated that exercise performance can be enhanced to a similar degree as a known caffeine dose. This 'placebo effect' phenomenon may be part of the mechanisms explaining caffeine's ergogenicity in exercise. However, there is no study that has established whether the placebo effect of caffeine is also present for other benefits obtained with acute caffeine intake, such as enhanced fat oxidation during exercise. Therefore, the aim of this investigation was to investigate the placebo effect of caffeine on fat oxidation during exercise. Twelve young men participated in a deceptive double-blind cross-over experiment. Each participant completed three identical trials consisting of a step incremental exercise test from 30 to 80% of V.O2max. In the two first trials, participants ingested either 3 mg/kg of cellulose (placebo) or 3 mg/kg of caffeine (received caffeine) in a randomized order. In the third trial, participants were informed that they had received 3 mg/kg of caffeine, but a placebo was provided (informed caffeine). Fat oxidation rates were derived from stoichiometric equations. In received caffeine, participants increased their rate of fat oxidation over the values obtained with the placebo at 30%, 40%, 50%, and 60% of V.O2max (all p < 0.050). In informed caffeine, participants increased their rate of fat oxidation at 30%, 40%, 50% 60%, and 70% of V.O2max (all p < 0.050) over the placebo, while there were no differences between received versus informed caffeine. In comparison to placebo (0.32 ± 0.15 g/min), the rate of maximal fat oxidation was higher in received caffeine (0.44 ± 0.22 g/min, p = 0.045) and in informed caffeine (0.41 ± 0.20 g/min, p = 0.026) with no differences between received versus informed caffeine. However, the intensity at which maximal fat oxidation rate was obtained (i.e., Fatmax) was similar in placebo, received caffeine, and informed caffeine trials (42.5 ± 4.5, 44.2 ± 9.0, and 41.7 ± 10.5% of V.O2max, respectively, p = 0.539). In conclusion, the expectancy of having received caffeine produced similar effects on fat oxidation rate during exercise than actually receiving caffeine. Therefore, the placebo effect of caffeine is also present for the benefits of acute caffeine intake on substrate oxidation during exercise and it may be used to enhance fat oxidation during exercise in participants while reducing any risks to health that this substance may have.
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Plasticity and heterogeneity of thermogenic adipose tissue.
Sun, W, Modica, S, Dong, H, Wolfrum, C
Nature metabolism. 2021;(6):751-761
Abstract
The perception of adipose tissue, both in the scientific community and in the general population, has changed dramatically in the past 20 years. While adipose tissue was thought for a long time to be a rather simple lipid storage entity, it is now recognized as a highly heterogeneous organ and a critical regulator of systemic metabolism, composed of many different subtypes of cells, with important endocrine functions. Additionally, adipose tissue is nowadays recognized to contribute to energy turnover, due to the presence of specialized thermogenic adipocytes, which can be found in many adipose depots. This review discusses the unprecedented insights that we have gained into the heterogeneity of thermogenic adipocytes and their respective precursors due to the technical developments in single-cell and nucleus technologies. These methodological advances have increased our understanding of how adipose tissue catabolic function is influenced by developmental and intercellular communication events.
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Pathophysiology of Obesity.
Kessler, C
The Nursing clinics of North America. 2021;(4):465-478
Abstract
As obesity continues a relentless march across the globe, researchers are beginning to unlock the complicated interplay among obesity, its ensuing inflammation, and downstream complications. It is becoming clear that obesity is a chronic, multifactorial, inflammatory disease of maladaptive adipose tissue mass involving complex links among genetics, hormonal-signaling, and the environment. Understanding the intricate pathogenesis of obesity and its sequela will go a long way to discovering better treatment options and lessen anti-obesity bias.
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Recent Advances in Adipose Tissue Dysfunction and Its Role in the Pathogenesis of Non-Alcoholic Fatty Liver Disease.
Wang, X, Rao, H, Liu, F, Wei, L, Li, H, Wu, C
Cells. 2021;(12)
Abstract
Obesity is a serious ongoing health problem that significantly increases the incidence of nonalcoholic fatty liver disease (NAFLD). During obesity, adipose tissue dysfunction is obvious and characterized by increased fat deposition (adiposity) and chronic low-grade inflammation. The latter has been implicated to critically promote the development and progression of NAFLD, whose advanced form non-alcoholic steatohepatitis (NASH) is considered one of the most common causes of terminal liver diseases. This review summarizes the current knowledge on obesity-related adipose dysfunction and its roles in the pathogenesis of hepatic steatosis and inflammation, as well as liver fibrosis. A better understanding of the crosstalk between adipose tissue and liver under obesity is essential for the development of new and improved preventive and/or therapeutic approaches for managing NAFLD.
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The Sick Adipose Tissue: New Insights Into Defective Signaling and Crosstalk With the Myocardium.
Bermúdez, V, Durán, P, Rojas, E, Díaz, MP, Rivas, J, Nava, M, Chacín, M, Cabrera de Bravo, M, Carrasquero, R, Ponce, CC, et al
Frontiers in endocrinology. 2021;:735070
Abstract
Adipose tissue (AT) biology is linked to cardiovascular health since obesity is associated with cardiovascular disease (CVD) and positively correlated with excessive visceral fat accumulation. AT signaling to myocardial cells through soluble factors known as adipokines, cardiokines, branched-chain amino acids and small molecules like microRNAs, undoubtedly influence myocardial cells and AT function via the endocrine-paracrine mechanisms of action. Unfortunately, abnormal total and visceral adiposity can alter this harmonious signaling network, resulting in tissue hypoxia and monocyte/macrophage adipose infiltration occurring alongside expanded intra-abdominal and epicardial fat depots seen in the human obese phenotype. These processes promote an abnormal adipocyte proteomic reprogramming, whereby these cells become a source of abnormal signals, affecting vascular and myocardial tissues, leading to meta-inflammation, atrial fibrillation, coronary artery disease, heart hypertrophy, heart failure and myocardial infarction. This review first discusses the pathophysiology and consequences of adipose tissue expansion, particularly their association with meta-inflammation and microbiota dysbiosis. We also explore the precise mechanisms involved in metabolic reprogramming in AT that represent plausible causative factors for CVD. Finally, we clarify how lifestyle changes could promote improvement in myocardiocyte function in the context of changes in AT proteomics and a better gut microbiome profile to develop effective, non-pharmacologic approaches to CVD.