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Differences in blood concentration of sex hormones in the follicular (FP) and luteal (LP) phases may influence energy metabolism in women. We compared fasting energy metabolism and sweet taste preference on a representative day of the FP and LP in twenty healthy women (25·3 (sd 5·1) years, BMI: 22·2 (sd 2·2) kg/m2) with regular self-reported menses and without the use of hormonal contraceptives. From the self-reported duration of the three prior menstrual cycles, the predicted FP and LP visits were scheduled for days 5–12 and 20–25 after menses, respectively. The order of the FP and LP visits was randomly assigned. On each visit, RMR and RQ by indirect calorimetry, sweet taste preference by the Monell two-series forced-choice tracking procedure, serum fibroblast growth factor 21 by a commercial ELISA (FGF21, a liver-derived protein with action in energy balance, fuel oxidation and sugar preference) and dietary food intake by a 24-h dietary recall were determined. Serum progesterone and oestradiol concentrations displayed the expected differences between phases. RMR was lower in the FP v. LP (5042 (sd 460) v. 5197 (sd 490) kJ/d, respectively; P = 0·04; Cohen effect size, d rm = 0·33), while RQ showed borderline significant higher values (0·84 (sd 0·05) v. 0·81 (sd 0·05), respectively; P = 0·07; d rm = 0·62). Also, in the FP v. LP, sweet taste preference was lower (12 (sd 8) v. 16 (sd 9) %; P = 0·04; d rm = 0·47) concomitant with higher serum FGF21 concentration (294 (sd 164) v. 197 (sd 104) pg/ml; P < 0·01; d rm = 0·66). The menstrual cycle is associated with changes in energy expenditure, sweet taste preference and oxidative fuel partitioning. [ABSTRACT FROM AUTHOR]

The emergence of chronic inflammation during obesity in the absence of overt infection or well-defined autoimmune processes is a puzzling phenomenon. The Nod-like receptor (NLR) family of innate immune cell sensors, such as the nucleotide- binding domain, leucine-rich-containing family, pyrin domain-containing-3 (Nlrp3, but also known as Nalp3 or cryopyrin) inflammasome are implicated in recognizing certain nonmicrobial originated 'danger signals' leading to caspase-1 activation and subsequent interleukin-1β (IL-1β) and IL-18 secretion. We show that calorie restriction and exercise-mediated weight loss in obese individuals with type 2 diabetes is associated with a reduction in adipose tissue expression of Nlrp3 as well as with decreased inflammation and improved insulin sensitivity. We further found that the Nlrp3 inflammasome senses lipotoxicity- associated increases in intracellular ceramide to induce caspase-1 cleavage in macrophages and adipose tissue. Ablation of Nlrp3 in mice prevents obesity-induced inflammasome activation in fat depots and liver as well as enhances insulin signaling. Furthermore, elimination of Nlrp3 in obese mice reduces IL-18 and adipose tissue interferon-γ (IFN-γ) expression, increases naive T cell numbers and reduces effector T cell numbers in adipose tissue. Collectively, these data establish that the Nlrp3 inflammasome senses obesity-associated danger signals and contributes to obesity-induced inflammation and insulin resistance., Despite the absence of any overt infection or definitive evidence of autoantigen-mediated immune cell activation during obesity, chronic inflammation in this state is an established instigator of several diseases such [...]

The overexpression of the adipose gene ( adp/WDTC1) in mice inhibits lipid accumulation and improves the metabolic profile. Objective Subcutaneous fat adp expression in humans and its relation to metabolic parameters was evaluated. Design and Methods Abdominal subcutaneous fat adp expression, insulin sensitivity (clamp), and respiratory quotient (RQ; indirect calorimetry) were assessed in: 36 obese and 56 BMI-, race-, and sex-matched type 2 diabetic volunteers (Look AHEAD Adipose Ancillary Study); 37 nondiabetic Pima Indians including obese ( n = 18) and nonobese ( n = 19) subjects and; 62 nonobese nondiabetic subjects at the Pennington Center in the ADAPT study. Results In the Look AHEAD Study, adp expression normalized for cyclophilin B was higher in males versus females (1.27 ± 0.06 vs. 1.11 ± 0.04; P < 0.01) but not after controlling for body fat. Adp expression was not influenced by the presence of diabetes but was related to body fat ( r = −0.23; P = 0.03), insulin sensitivity ( r = 0.23; P = 0.03) and fasting/insulin-stimulated RQ ( r = 0.31 and 0.33; P < 0.01). In Pima Indians, adp expression was also higher in males versus females (1.00 ± 0.05 vs. 0.77 ± 0.05; P = 0.02) and higher in nonobese versus obese (1.02 ± 0.05 vs. 0.80 ± 0.06; P = 0.03). In the ADAPT study, there was no difference in adp expression between males and females. Conclusion Consistent with animal studies, our results suggest that high adp expression in human adipose tissue is associated with lower adiposity and enhanced glucose utilization. [ABSTRACT FROM AUTHOR]

The authors reflect on the results of a study that appeared in the journal "Obesity" which examined the effect of visceral fat on insulin resistance in the canine model. They explain that the study considered the effect of increasing canine ornamental fat through pharmacological sympathectomy on insulin sensitivity and found that visceral fat per se does not result in insulin resistance. They argue that the results may not be suitable for testing the portal hypothesis.

Objective: the aim of this study was to analyze the agreement between the resting energy expenditure (REE) obtained by indirect calorimetry (IC) and that obtained by prediction equations in a sample of healthy adults from Spain. Méthods: a descriptive cross-sectional study was conducted in 95 healthy, normal-weight adults. REE was determined by IC and 45 population-specific prediction equations which were based on weight, height, sex and/or body composition (BC). The Intraclass Correlation Coefficient (ICC) and Bland-Alman plots were used to analyze the agreement between the REE obtained by IC and that obtained by prediction equations. The level of signification was reached at p < 0,05. Results: mean age was 42 years (range: 23.0-63.2). Mean REE determined by CI was 1589 (312) kcal/d [1822.3 (224.3) kcal/d in men and 1379.3 (216.1) kcal/d in women; p < 0.05]. The De-Lorenzo, Harris-Benedict, Schofield, and especially the Korth equations showed the greatest level of agreement with respect to IC. Conclusions: there is high variability in the estimates of REE depending on the prediction equation used. The De Lorenzo, Harris-Benedict, and the Schofield equations showed a good level of agreement in our sample; however, the Korth equation was the most appropriate. Equations based on weight and/or height were more accurate than those which included body composition variables. [ABSTRACT FROM AUTHOR]

Capsinoids are non-pungent compounds with molecular structures similar to capsaicin, which has accepted thermogenic properties. To assess the acute effect of a plant-derived preparation of capsinoids on energy metabolism, we determined RMR and non-protein respiratory quotient (NPRQ) after ingestion of different doses of the capsinoids. Thirteen healthy subjects received four doses of the capsinoids (1, 3, 6 and 12 mg) and placebo using a crossover, randomised, double-blind trial. After a 10 h overnight fast as inpatients, RMR was measured by indirect calorimetry for 45 min before and 120 min after ingesting capsinoids or placebo. Blood pressure and axillary temperature were measured before ( - 55 and - 5 min) and after (60 and 120 min) dosing. Before dosing, mean RMR was 6247 (se 92) kJ/d and NPRQ was 0.86 (se 0.01). At 120 min after dosing, metabolic rate and NPRQ remained similar across the four capsinoids and placebo doses. Capsinoids also had no influence on blood pressure or axillary temperature. Capsinoids provided in four doses did not affect metabolic rate and fuel partitioning in human subjects when measured 2 h after exposure. Longer exposure and higher capsinoids doses may be required to cause meaningful acute effects on energy metabolism.

Metabolic flexibility is the capacity for the organism to adapt fuel oxidation to fuel availability. The inability to modify fuel oxidation in response to changes in nutrient availability has been implicated in the accumulation of intramyocellular lipid and insulin resistance. The metabolic flexibility assessed by the ability to switch from fat to carbohydrate oxidation is usually impaired during a hyperinsulinemic clamp in insulin-resistant subjects; however, this "metabolic inflexibility" is mostly the consequence of impaired cellular glucose uptake. Indeed, after controlling for insulin-stimulated glucose disposal rate (amount of glucose available for oxidation), metabolic flexibility is not altered in obesity regardless of the presence of type 2 diabetes. To understand how intramyocellular lipids accumulate and cause insulin resistance, the assessment of metabolic flexibility to high-fat diets is more relevant than metabolic flexibility during a hyperinsulinemic clamp. An impaired capacity to upregulate muscle lipid oxidation in the face of high lipid supply may lead to increased muscle fat accumulation and insulin resistance. Surprisingly, very few studies have investigated the response to high-fat diets. In this review, we discuss the role of glucose disposal rate, adipose tissue lipid storage, and mitochondrial function on metabolic flexibility. Additionally, we emphasize the bias of using the change in respiratory quotient to calculate metabolic flexibility and propose novel approaches to assess metabolic flexibility. On the basis of current evidence, one cannot conclude that impaired metabolic flexibility is responsible for the accumulation of intramyocellular lipid and insulin resistance. We propose to study metabolic flexibility in response to high-fat diets in individuals having contrasting degree of insulin sensitivity and/or mitochondrial characteristics.