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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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Green Tea, Intermittent Sprinting Exercise, and Fat Oxidation.
Gahreman, D, Wang, R, Boutcher, Y, Boutcher, S
Nutrients. 2015;(7):5646-63
Abstract
Fat oxidation has been shown to increase after short term green tea extract (GTE) ingestion and after one bout of intermittent sprinting exercise (ISE). Whether combining the two will result in greater fat oxidation after ISE is undetermined. The aim of the current study was to investigate the combined effect of short term GTE and a single session of ISE upon post-exercise fat oxidation. Fourteen women consumed three GTE or placebo capsules the day before and one capsule 90 min before a 20-min ISE cycling protocol followed by 1 h of resting recovery. Fat oxidation was calculated using indirect calorimetry. There was a significant increase in fat oxidation post-exercise compared to at rest in the placebo condition (p < 0.01). After GTE ingestion, however, at rest and post-exercise, fat oxidation was significantly greater (p < 0.05) than that after placebo. Plasma glycerol levels at rest and 15 min during post-exercise were significantly higher (p < 0.05) after GTE consumption compared to placebo. Compared to placebo, plasma catecholamines increased significantly after GTE consumption and 20 min after ISE (p < 0.05). Acute GTE ingestion significantly increased fat oxidation under resting and post-exercise conditions when compared to placebo.
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Soluble CD163 is associated with CD163 mRNA expression in adipose tissue and with insulin sensitivity in steady-state condition but not in response to calorie restriction.
Kračmerová, J, Rossmeislová, L, Kováčová, Z, Klimčáková, E, Polák, J, Tencerová, M, Mališová, L, Štich, V, Langin, D, Šiklová, M
The Journal of clinical endocrinology and metabolism. 2014;(3):E528-35
Abstract
CONTEXT Soluble CD163 (sCD163) was suggested as a biomarker of insulin sensitivity and CD163 mRNA expression representing macrophage content in adipose tissue (AT). OBJECTIVE The aim of this study was to investigate, in cross-sectional and prospective design, the relationship between sCD163 circulating levels and CD163 mRNA expression in adipose tissue and insulin sensitivity assessed by euglycemic-hyperinsulinemic clamp. DESIGN, SETTING, PARTICIPANTS, AND INTERVENTIONS Two cohorts of subjects were examined in the study. Cohort 1 included 42 women with a wide range of body mass index (17-48 kg/m(2)); cohort 2 included 27 obese women who followed a dietary intervention consisting of 1 month of a very low-calorie diet and 5 months of a weight-stabilization period. MAIN OUTCOME MEASURES Serum levels of CD163 and mRNA expression of CD163 and CD68 in sc and visceral (visc) AT were determined, and insulin sensitivity [expressed as glucose disposal rate (GDR)] was measured in cohort 1. In cohort 2, serum levels of CD163, mRNA expressions of CD163, CD68, and CD163-shedding factors [TNF-α-converting enzyme (TACE) and tissue inhibitor of metalloproteinase (TIMP3)] in sc AT were examined and GDR was measured before and during dietary intervention. RESULTS In cohort 1, circulating sCD163 correlated with CD163 mRNA levels in both sc and visc AT. sCD163 and CD163 mRNA expression in both fat depots correlated with GDR. In cohort 2, the diet-induced changes of sCD163 levels did not correlate with those of CD163, CD68, TACE, and TIMP3 mRNA levels. Although the pattern of the diet-induced change of sCD163 paralleled that of GDR, there was no correlation between the changes of these two variables. CONCLUSION sCD163 correlates with CD163 mRNA expression in sc and visc AT and with whole-body insulin sensitivity in the steady-state condition. These associations are not observed with respect to the diet-induced changes during a weight-reducing hypocaloric diet.
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Epicardial adipose tissue thickness in hemodialysis patients.
Altun, B, Tasolar, H, Eren, N, Binnetoğlu, E, Altun, M, Temiz, A, Gazi, E, Barutcu, A, Altunoren, O, Colkesen, Y, et al
Echocardiography (Mount Kisco, N.Y.). 2014;(8):941-6
Abstract
AIM: Hemodialysis (HD) patients had higher cardiovascular mortality and it is related to atherosclerosis. Epicardial adipose tissue (EAT) thickness is a marker of atherosclerosis and independent predictor of coronary artery disease. The aim of our study was to evaluate the relationship between EAT and carotid intima-media thickness (CIMT) predictors of early atherosclerosis in HD patients. METHODS The study included 62 HD patients and 40 healthy controls. EAT thickness and CIMT were measured by echocardiography in all subjects. RESULTS Epicardial adipose tissue thickness and CIMT were higher (6.98 ± 1.67 vs. 3.84 ± 0.73 mm, P < 0.001, 0.94 ± 0.17 vs. 0.63 ± 0.11 mm, P < 0.001, respectively) in HD patients than in control subjects. EAT thickness were correlated with CIMT, HD duration, age, and calcium. In addition, HD duration, CIMT, and age were independent predictors of EAT thickness on HD patients in regression analysis. CONCLUSION Epicardial adipose tissue thickness may be a useful indicator of early atherosclerosis in HD patients.
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Comparison of bioimpedance and dual-energy x-ray absorptiometry for measurement of fat mass in hemodialysis patients.
Molfino, A, Don, BR, Kaysen, GA
Nephron. Clinical practice. 2012;(3-4):127-33
Abstract
BACKGROUND Fat mass (FM) is measured with dual-energy X-ray absorptiometry (DXA), but is expensive and not portable. Multifrequency bioimpedance spectroscopy (BIS) measures total body water (TBW), intracellular water (ICW) and extracellular water (ECW). FM is calculated by subtracting fat-free mass (FFM) from weight assuming a fractional hydration of FFM of 0.73. Hemodialysis (HD) patients, however, have nonphysiologic expansion of ECW. Our aim was to apply a model to estimate FM in HD patients and controls. METHODS We estimated the hydration of FFM in healthy subjects and HD patients with BIS (Impedimed multifrequency) assuming a hydration of 0.73 or using a model allowing ECW and ICW to vary, deriving a value for FM accounting for variances in ECW and ICW. FM was measured by DXA (Hologic Discovery W) in 25 controls and in 11 HD patients. We measured TBW, ECW and ICW with BIS and calculated FM using either weight - TBW/0.73 or with a model accounting for variations in ECW/ICW to estimate FM. RESULTS ECW/ICW was greater in HD patients than in controls (0.83 ± 0.08 vs. 0.76 ± 0.04; p = 0.001). FM (kg) measured by DXA or estimated from TBW using constant hydration or accounting for variations in ECW/ICW was not significantly different in controls or in HD patients. Values obtained by all methods correlated (p < 0.001) and none of the Bland-Altman plots regressed (r(2) = 0.00). FM measured by DXA and by BIS in both controls and HD patients combined correlated (r(2) = 0.871). CONCLUSION Expansion of ECW in HD patients is statistically significant; however, the effect on hydration of FFM was insufficient to cause significant deviation from values derived using a hydration value of 0.73 within the range of expansion of ECW in the HD patient population studied here.
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Pharmacokinetic pilot study of the antiangiogenic activity of standardized platycodi radix.
Twiner, EM, Liu, Z, Gimble, J, Yu, Y, Greenway, F
Advances in therapy. 2011;(10):857-65
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Abstract
INTRODUCTION Platycodi radix is a radish used in food, such as Korean kimchi, and has been shown to cause weight loss in rodents. Platycodin D is considered its active ingredient and has been shown to inhibit lipases. The authors hypothesized that platycodi radix and the platycodin D it contains inhibit angiogenesis; another mechanism for weight loss. METHODS This study tested platycodi radix extract, platycodin D, and an extract of platycodi radix standardized to platycodin D for their ability to inhibit angiogenesis in a human adipose tissue assay. This study treated five healthy volunteers, orally, with platycodi radix extract standardized to 414 mg of platycodin D. Three volunteers were treated under fasting conditions, one volunteer with a 400 kcal meal, and one volunteer treated with a placebo. Blood was drawn over 5 hours to compare serum inhibition of the human adipose tissue angiogenesis. RESULTS Platycodin radix extract, platycodin D, and platycodi radix extract standardized to platycodin D all inhibited angiogenesis. The three volunteers who consumed platycodi radix extract standardized to 414 mg of platycodin D had a 25.76% reduction in angiogenesis from baseline at 60 minutes (P<0.002), and had a statistically significant reduction in angiogenesis from 30 to 240 minutes (P<0.05 to P<0.002). The placebo decreased angiogenesis by 5.6% between 30 and 240 minutes, compared with 17.8% by the extract. The meal delayed absorption by approximately 3.5 hours. CONCLUSION Platycodi radix extract standardized to platycodin D inhibited angiogenesis in human volunteers, and paves the way for a dose-response study and a human clinical obesity trial.
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Does the DASH diet lower blood pressure by altering peripheral vascular function?
Hodson, L, Harnden, KE, Roberts, R, Dennis, AL, Frayn, KN
Journal of human hypertension. 2010;(5):312-9
Abstract
We tested whether lowering of blood pressure (BP) on the dietary approaches to stop hypertension (DASH) diet was associated with changes in peripheral vascular function: endothelial function, assessed by flow-mediated vasodilatation (FMD) of the brachial artery, and subcutaneous adipose tissue blood flow (ATBF). We also assessed effects on heart rate variability (HRV) as a measure of autonomic control of the heart. We allocated 27 men and women to DASH diet and control groups. We measured FMD, ATBF and HRV on fasting and after ingestion of 75 g glucose, before and after 30 days on dietary intervention, aiming for weight maintenance. The control group did not change their diet. The DASH-diet group complied with the diet as shown by significant reductions in systolic (P<0.001) and diastolic (P=0.005) BP, and in plasma C-reactive protein (P<0.01), LDL-cholesterol (P<0.01) and apolipoprotein B (P=0.001), a novel finding. Body weight changed by <1 kg. There were no changes in the control group. We found no changes in FMD, or in ATBF, in the DASH-diet group, although heart rate fell (P<0.05). Glucose and insulin concentrations did not change. In this small-scale study, the DASH diet lowered BP independently of peripheral mechanisms.
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Assessment of non-insulin-mediated glucose uptake: association with body fat and glycemic status.
Jumpertz, R, Thearle, MS, Bunt, JC, Krakoff, J
Metabolism: clinical and experimental. 2010;(10):1396-401
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In the fasting state, approximately 83% of glucose uptake occurs via non-insulin-mediated mechanisms. A widely accepted static rate for NIMGU is 1.62 mg kg(-1)·min(-1). To investigate the variability of NIMGU, we examined differences by glucose tolerance, sex, age, race (American Indian/African American/Caucasian), and adiposity in 616 volunteers (including individuals with normal glucose regulation [NGR] and impaired glucose regulation [IGR] and diabetes mellitus [DM]) using data from euglycemic-hyperinsulinemic clamp experiments. NIMGU was determined by plotting basal glucose output and insulin action against fasting and steady-state clamp insulin. The intercept with the y-axis after extrapolation was interpreted as NIMGU at zero insulin. Body composition was determined by dual-energy x-ray absorptiometry; and glucose regulation, by a 75-g oral glucose tolerance test. Energy expenditure was measured by indirect calorimetry in a metabolic chamber. In individuals with NGR (n = 385), NIMGU was 1.63 mg kg(estimated metabolic body size (fat free mass + 17.7 kg))(-1) min(-1) (95% confidence interval, 1.59-1.66). NIMGU increased with IGR and DM (IGR: n = 189, 1.67 [1.62-1.72]; DM: n = 42, 2.39 [2.29-2.49]; P < .0001 across groups). NIMGU did not differ by sex (P = .13), age (P = .22), or race (P = .06); however, NIMGU was associated with percentage body fat (r(2) = 0.04, P < .0001). Furthermore, NIMGU was positively associated with 24-hour and sleep energy expenditure (r(2) = 0.002, P = .03; r(2) = 0.01, P < .01). Extrapolated NIMGU in individuals with NGR is remarkably consistent with previously published data. Our results indicate that NIMGU is associated with adiposity. NIMGU increases with declining glucose tolerance perhaps to preserve glucose uptake during increased insulin resistance.
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Restoration of muscle mitochondrial function and metabolic flexibility in type 2 diabetes by exercise training is paralleled by increased myocellular fat storage and improved insulin sensitivity.
Meex, RC, Schrauwen-Hinderling, VB, Moonen-Kornips, E, Schaart, G, Mensink, M, Phielix, E, van de Weijer, T, Sels, JP, Schrauwen, P, Hesselink, MK
Diabetes. 2010;(3):572-9
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OBJECTIVE Mitochondrial dysfunction and fat accumulation in skeletal muscle (increased intramyocellular lipid [IMCL]) have been linked to development of type 2 diabetes. We examined whether exercise training could restore mitochondrial function and insulin sensitivity in patients with type 2 diabetes. RESEARCH DESIGN AND METHODS Eighteen male type 2 diabetic and 20 healthy male control subjects of comparable body weight, BMI, age, and VO2max participated in a 12-week combined progressive training program (three times per week and 45 min per session). In vivo mitochondrial function (assessed via magnetic resonance spectroscopy), insulin sensitivity (clamp), metabolic flexibility (indirect calorimetry), and IMCL content (histochemically) were measured before and after training. RESULTS Mitochondrial function was lower in type 2 diabetic compared with control subjects (P = 0.03), improved by training in control subjects (28% increase; P = 0.02), and restored to control values in type 2 diabetic subjects (48% increase; P < 0.01). Insulin sensitivity tended to improve in control subjects (delta Rd 8% increase; P = 0.08) and improved significantly in type 2 diabetic subjects (delta Rd 63% increase; P < 0.01). Suppression of insulin-stimulated endogenous glucose production improved in both groups (-64%; P < 0.01 in control subjects and -52% in diabetic subjects; P < 0.01). After training, metabolic flexibility in type 2 diabetic subjects was restored (delta respiratory exchange ratio 63% increase; P = 0.01) but was unchanged in control subjects (delta respiratory exchange ratio 7% increase; P = 0.22). Starting with comparable pretraining IMCL levels, training tended to increase IMCL content in type 2 diabetic subjects (27% increase; P = 0.10), especially in type 2 muscle fibers. CONCLUSIONS Exercise training restored in vivo mitochondrial function in type 2 diabetic subjects. Insulin-mediated glucose disposal and metabolic flexibility improved in type 2 diabetic subjects in the face of near-significantly increased IMCL content. This indicates that increased capacity to store IMCL and restoration of improved mitochondrial function contribute to improved muscle insulin sensitivity.
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Differential expression of aquaporin 7 in adipose tissue of lean and obese high fat consumers.
Marrades, MP, Milagro, FI, Martínez, JA, Moreno-Aliaga, MJ
Biochemical and biophysical research communications. 2006;(3):785-9
Abstract
Aquaporin 7 (AQP7) is an aquaglyceroprotein responsible for the secretion and uptake of glycerol from the adipocyte. The modulation of the expression of this membrane transport protein might play an important role in the susceptibility to the development of obesity. The aim of the present study was to compare the AQP7 gene expression in subcutaneous abdominal fat in lean vs. obese high fat intakers with a similar daily physical activity pattern. Twelve young men, 6 lean (BMI=23.2+/-0.4kg/m(2)) and 6 obese (35.0+/-1.1kg/m(2)) with a similar habitual dietary intake of fat (45.5+/-2.5 vs. 43.5+/-1.7% daily energy from fat for lean and obese, respectively) and physical activity (16.0+/-5.7 vs. 17.2+/-5.1 METsh/week for lean and obese, respectively), were recruited. Subcutaneous abdominal fat biopsies were obtained and total RNA was extracted and purified. Pools of RNA from lean and obese individuals were probed into Affymetrix GeneChip Human U133A. The microarray analysis revealed that AQP7 gene was down-regulated in obese compared to lean subjects. The results of the microarray analysis were confirmed by real-time PCR studies. In summary, our data show that the AQP7 gene is differentially expressed in adipose tissue of lean and obese individuals. The down-regulation of the AQP7 gene could be implicated in the susceptibility to obesity by reducing glycerol release and promoting the accumulation of lipids in the adipose tissue.