Thermic Effect Research Articles

Sympathetic blockade on diet induced thermogenesis in the congenic LA/Ntul//-cp rat

The effects of overfeeding highly palatable diets via the cafeteria feeding diet method (Café) has been shown to be a reliable experimental model to induce diet induced thermogenesis (DIT) in young adult normally lean rats of several strains. Groups of young adult lean LA/ Ntul//-cp rats were offered a Purina chow diet (CHOW) or the same diet plus a daily café supplement both ad libitum from 10 until 24 weeks of age. The drug α-methylparatyrosine (α-MPT) was administered to groups (250 mg α-MPT/kg BW, i.p.) to ablate sympathetic (SNS) activity or a sham injection of physiologic saline given, and measures of fasting resting thermogenesis obtained at thermal neutrality (30°C) before and after the α-MPT or sham administration. The Café diet resulted in a 67% increase in body weight (BW) and a ~25% increase in resting oxygen consumption (VO2) following café overfeeding in both groups, while only a 40% increase in BW and no additional increase in VO2 occurred in normally CHOW fed rats while the sham injection was without any variations from normal physiologic responses as predicted. Sympathetic blockade with α-MPT was associated with modest decreases in body temperature and an average ~12-15% decrease in VO2 in the café treated group, but when the VO2 data were arithmetically corrected to isothermal conditions only a net 3% decrease occurred in CHOW fed rats and was without effect on the SHAM group. Serum T3 concentrations increased by 92% and urinary catecholamine excretion of VMA >250% following the café diet, but the urinary vanilmandelic acid (VMA) excretion was virtually nil following the sympathetic blockade. These observations indicate that the SNS-mediated contribution component to DIT following prolonged café overfeeding under conditions of thermal neutrality contribute approximately 50% of the thermic response. While under normal long term CHOW feeding the SNS component may be as little as 3% of the thermic response, and thus, the total thermic response of DIT likely represents a combination of short acting SNS and longer acting non-SNS mechanisms, including a likely significant thyroidal component in normally lean animals.

First identification, chemical analysis and pharmacological characterization of N-piperidinyl etonitazene (etonitazepipne), a recent addition to the 2-benzylbenzimidazole opioid subclass.

N-Piperidinyl etonitazene ('etonitazepipne') represents a recent addition to the rapidly expanding class of 2-benzylbenzimidazole 'nitazene' opioids. Following its first identification in an online-sourced powder and in biological samples from a patient seeking help for detoxification, this report details its in-depth chemical analysis and pharmacological characterization. Analysis of the powder via different techniques (LC-HRMS, GC-MS, UHPLC-DAD, FT-IR) led to the unequivocal identification of N-piperidinyl etonitazene. Furthermore, we report the first activity-based detection and analytical identification of N-piperidinyl etonitazene in authentic samples. LC-HRMS analysis revealed concentrations of 1.21ng/mL in serum and 0.51ng/mL in urine, whereas molecular networking enabled the tentative identification of various (potentially active) urinary metabolites. In addition, we determined that the extent of opioid activity present in the patient's serum was equivalent to the in vitro opioid activity exerted by 2.5-10ng/mL fentanyl or 10-25ng/mL hydromorphone in serum. Radioligand binding assays in rat brain tissue revealed that the drug binds with high affinity (Ki = 14.3nM) to the µ-opioid receptor (MOR). Using a MOR-β-arrestin2 activation assay, we found that N-piperidinyl etonitazene is highly potent (EC50 = 2.49nM) and efficacious (Emax = 183% versus hydromorphone) in vitro. Pharmacodynamic evaluation in male Sprague Dawley rats showed that N-piperidinyl etonitazene induces opioid-like antinociceptive, cataleptic, and thermic effects, its potency in the hot plate assay (ED50 = 0.0205mg/kg) being comparable to that of fentanyl (ED50 = 0.0209mg/kg), and > 190 times higher than that of morphine (ED50 = 3.940mg/kg). Taken together, our findings indicate that N-piperidinyl etonitazene is a potent opioid with the potential to cause harm in users.

Maternal High-Fructose Intake Activates Myogenic Program in Fetal Brown Fat and Predisposes Offspring to Diet-Induced Metabolic Dysfunctions in Adulthood.

Excess dietary fructose intake is a major public health concern due to its deleterious effect to cause various metabolic and cardiovascular diseases. However, little is known about the effects of high-fructose consumption during pregnancy on offspring metabolic health in adulthood. Here, we show that maternal consumption of 20% (w/v) fructose water during pregnancy does not alter the metabolic balance of offspring with a chow diet, but predisposes them to obesity, fatty liver, and insulin resistance when challenged by a high-fat diet. Mechanistically, diet-induced brown fat reprogramming and global energy expenditure in offspring of fructose-fed dams are impaired. RNA-seq analysis of the fetal brown fat tissue reveals that the myogenic pathway is predominantly upregulated in the fructose-treated group. Meanwhile, circulating fructose level is found to be significantly elevated in both fructose-fed dams and their fetuses. Importantly fructose gavage also acutely activates the myogenic program in mice brown fat. Together, our data suggest that maternal high-fructose intake impairs fetal brown fat development, resultantly attenuates diet-induced thermogenesis and causes metabolic disorders in adult offspring probably through inducing myogenic signature in brown fat at the fetal stage.

Integrated proteome and phosphoproteome analysis of interscapular brown adipose and subcutaneous white adipose tissues upon high fat diet feeding in mouse

Thermogenesis is a promising approach to limit weight gain in response to excess nutrition. In contrast to cold-induced thermogenesis, the molecular and cellular mechanisms of diet-induced thermogenesis (DIT) have not been fully characterized. Here, we explored the response of brown adipose tissue (BAT) and subcutaneous white adipose tissue (sWAT) to high fat diet (HFD) using proteome and phosphoproteome analysis. We observed that after HFD, Uncoupling protein 1 (UCP1) and its phosphorylation were only increased in BAT. Furthermore, proteins involved in fatty acid oxidation, tricarboxylic acid cycle, and oxidative phosphorylation were also upregulated in BAT. Nevertheless, most metabolic related proteins were downregulated in sWAT. We found that these metabolic changes accompanied with different variation of mitochondrial proteins between BAT and sWAT. After HFD, most mitochondrial proteins were decreased in sWAT, but not in BAT. This effect was correlated with decreased mitochondrial ribosomal proteins in sWAT. Finally, through phosphoproteomic analysis, we predicted the activities of kinases in HFD mice and observed that there were more kinases inactivated in sWAT. Finally, this dataset provides a valuable resource for molecular researchers in the fields of obesity and obesity-related disease. SignificanceThermogenesis is a promising approach to combat obesity in response to excess energy. Nevertheless, the molecular and cellular mechanisms of DIT have not been fully characterized. Herein, we employed mass spectrometry (MS)-based proteomics and phosphoproteomics to identify differentially regulated proteins and phosphosites in BAT and sWAT of mice fed with HFD. This study unveils the differential regulatory networks of HFD in BAT and sWAT, which provides reference omics data to future researchers.

Infrared Efficiency and Ultraviolet Management of Red-Pigmented Polymethylmethacrylate Photoselective Greenhouse Films.

Red-pigmented photoselective polymethylmethacrylate (PMMA) films were prepared by casting from polymer/chloroform solution. The films were doped with efficient red fluorescent perylene dyes specialized for plastic coloration, namely KREMER 94720 and KREMER 94739, which have excellent weathering stability and a high fluorescence quantum yield. The effect of the doping concentration was studied using the atomic force microscope (AFM), optical transmission, color measurement, time-resolved fluorescence, and Fourier transform infrared spectroscopy (FTIR). The obtained results suggested the potential usefulness for photoselective greenhouse cladding applications as the lowest doping concentration (10−5 wt%) displaying the UV-open effect, whereas the best UV-blocking and thermic effects were obtained for the highest doping concentration (10−1 wt).

Increased Salt Intake Decreases Diet-Induced Thermogenesis in Healthy Volunteers: A Randomized Placebo-Controlled Study.

High salt intake ranks among the most important risk factors for noncommunicable diseases. Western diets, which are typically high in salt, are associated with a high prevalence of obesity. High salt is thought to be a potential risk factor for obesity independent of energy intake, although the underlying mechanisms are insufficiently understood. A high salt diet could influence energy expenditure (EE), specifically diet-induced thermogenesis (DIT), which accounts for about 10% of total EE. We aimed to investigate the influence of high salt on DIT. In a randomized, double-blind, placebo-controlled, parallel-group study, 40 healthy subjects received either 6 g/d salt (NaCl) or placebo in capsules over 2 weeks. Before and after the intervention, resting EE, DIT, body composition, food intake, 24 h urine analysis, and blood pressure were obtained. EE was measured by indirect calorimetry after a 12 h overnight fast and a standardized 440 kcal meal. Thirty-eight subjects completed the study. Salt intake from foods was 6 g/d in both groups, resulting in a total salt intake of 12 g/d in the salt group and 6 g/d in the placebo group. Urine sodium increased by 2.29 g/d (p < 0.0001) in the salt group, indicating overall compliance. The change in DIT differed significantly between groups (placebo vs. salt, p = 0.023). DIT decreased by 1.3% in the salt group (p = 0.048), but increased by 0.6% in the placebo group (NS). Substrate oxidation indicated by respiratory exchange ratio, body composition, resting blood pressure, fluid intake, hydration, and urine volume did not change significantly in either group. A moderate short-term increase in salt intake decreased DIT after a standardized meal. This effect could at least partially contribute to the observed weight gain in populations consuming a Western diet high in salt.

Impact of isoenergetic intake of irregular meal patterns on thermogenesis, glucose metabolism, and appetite: a randomized controlled trial

Evidence is emerging that interdaily meal pattern variability potentially affects response such as thermic effect of food (TEF), macronutrient metabolism, and appetite. To investigate the effect of irregular meal pattern on TEF, glucose, insulin, lipid profile, and appetite regulation in women who are overweight or with obesity and confirmed insulin resistance. In a randomized crossover trial, 9 women [mean ± SD BMI (in kg/m2): 33.3 ± 3.1] with confirmed insulin resistance consumed a regular (14 d; 6 meals/d) and an irregular (14 d; 3-9 meals/d) meal pattern separated by a 14-d washout interval. Identical foods were provided during the interventions, and at the start and end of each meal pattern, participants attended the laboratory after an overnight fast. Energy expenditure, glucose, insulin, lipids, adiponectin, leptin, glucagon-like peptide 1 (GLP-1), peptide YY (PYY), and ghrelin were measured at baseline and for 3 h after consumption of a test drink, after which an ad libitum test meal was offered. Subjective appetite ratings were recorded before and after the test drink, after the ad libitum meal, and during the intervention. Continuous interstitial glucose monitoring was undertaken for 7 consecutive days during each intervention. TEF (over 3 h) was significantly lower postirregular intervention compared with postregular (97.7 ± 19.2 kJ*3 h in postregular visit and 76.7 ± 35.2 kJ*3 h in postirregular visit, paired t test, P = 0.048). Differences in HOMA-IR between the 2 interventions (3.3 ± 1.7 and 3.6 ± 1.6 in postregular and postirregular meal pattern, respectively) were not significant. Net incremental AUC for GLP-1 concentrations (over 3 h) for the postregular meal pattern were higher (864.9 ± 456.1 pmol/L*3 h) than the postirregular meal pattern (487.6 ± 271.7 pmol/L*3 h, paired t test, P = 0.005). Following a 14-d period of an irregular meal pattern, TEF was significantly less than following a regular meal pattern, potentially compromising weight management if sustained long term. This study was registered at www.clinicaltrials.gov as NCT02582606.

Treatment with α-Methylparatyrosine Inhibits Sympathetic but Not Thyroidal Responses to Diet-Induced Thermogenesis in Lean Cafeteria-Overfed Rats

The sympathoplegic drug α-methylparatyrosine (α-MPT) was administered to lean, normally fed rats or rats overfed to induce diet induced thermogenesis (DIT) with a highly palatable Cafeteria diet regimen (Café) for twelve weeks, and measures of resting thermogenesis under thermoneutral conditions (VO2 at ambient 30°C), serum T3 and 24-hour urinary vanilmandelic acid (VMA) excretion determined before and after the α-MPT treatment. The café diet resulted in significant increases in VO2, serum T3, and VMA excretion. The α-MPT resulted in approximately fifty percent decrease in the Café-induced increase in VO2 after 24hours, while thyroidal function appeared clinically unaffected. These observations suggest that the sympathetic contributions to diet-induced thermogenesis (DIT) following chronic overfeeding with the Café diet regimen represent only about half of the reported dietary induced thermic response to overfeeding and non-sympathetic contributions including the thyroidal actions that likely account for the remaining proportion of the increased DIT and sympathetic component may decrease further over time spent since feeding.

Diet-Induced Thermogenesis: Principles and Pitfalls.

Concerning diet-induced thermogenesis, methodological issues relate mainly to the interpretation of measurements, rather than to the technical methodology as such. In the following, we point to a series of issues where the analysis often suggests the occurrence of UCP1-related diet-induced thermogenesis but where the observations areoften the consequences of a process that has induced leanness ratherthan being the cause of them. We particularly emphasize the necessity of focusing on the totalorganism when interpreting biochemical and molecular data, where the concept of total tissue values rather than relative data better reflects physiologically important alterations. We stress the importance of performing experiments at thermoneutrality in order to obtain clinically relevant data and stress that true thermogenic agents may be overlooked if this is not done.

Sufficiently Elevated Core Body Temperature May Be Necessary to Maintain Cerebral Blood Flow Response throughout the Morning

In comparison to a carbohydrate-rich breakfast, a nutritionally balanced breakfast reportedly leads to a higher core body temperature because of diet-induced thermogenesis (DIT) and also results in higher task performance. This study aimed to examine the relationships among the core body temperature, blood glucose level, cerebral blood flow, and cognitive performance when the core body temperature is raised to a similar extent as in DIT in the morning. This crossover study included 18 male participants who performed four sets of cognitive tests in the morning with four different foot baths and glucose intake conditions. In elevated body temperature (EBT) conditions, the core body temperature was increased by a foot bath at 42˚C or 39˚C, while in low body temperature (LBT) conditions, it was maintained at 35˚C by a foot bath; the participants received no glucose or two intakes of 20-g glucose for each thermal condition. In addition to the core body temperature measurement, the cerebral blood flow in the dorsolateral prefrontal cortex (DLPFC) was measured using near-infrared spectroscopy. Three blood collections were performed to measure the changes in blood glucose levels. The results revealed that in the EBT conditions, the core body temperature remained 0.3˚C - 0.5˚C higher than that at wake-up time, while the glucose intake conditions increased blood glucose levels which remained higher than those during fasting. No significant between-treatment difference was observed in the results of cognitive tests. However, the blood flow in the DLPFC increased during the second test period in the EBT/glucose and LBT/glucose conditions, whereas during the fourth test period, it increased solely in the EBT/glucose condition. Thus, in addition to the blood glucose level, an elevated core body temperature within the physiological range may be needed for long-term maintenance of the cerebral blood flow response.

Nardilysin in hepatocyte regulates diet-induced thermogenesis via the modulation of brown adipose tissue activity

Nardilysin in hepatocyte regulates diet-induced thermogenesis via the modulation of brown adipose tissue activity

Alimentación basada en plantas: sus mecanismos en la prevención y tratamiento de la obesidad

Obesity is a metabolic condition with a continuous increasing rate, being considered today a “pandemic”. Due to this and the vast number of diseases it is associated with, there is a need for a treatment of this condition that is both effective and healthy in a comprehensive way. In this context, the concepts of lifestyle medicine and plant-based diets have emerged in medicine and in scientific research, and the latter have demonstrated benefits in all these areas and are being part of several scientific association’s recommendations today. In this article, a plant-based diet is briefly defined, and the mechanisms by which this type of diet provides benefits for the control of body weight are explored, including the satiety it generates and its characteristic low caloric density, the higher thermic effect of foods, the positive modulation of the gut microbiota, its effects on the insulin sensitivity, the absence of animal protein and how this affects the body weight, and the effects it has on the leptin hormone. Plant-based diets has been studied both in observational and interventional studies and positioned as a great alternative for the prevention and treatment of obesity, in addition to being a safe and health dietary pattern. We hope that in the future, more health professionals consider this evidence and incorporate it as part of their therapeutic tools.

CO2 emission rates from sedentary subjects under controlled laboratory conditions

We determined carbon dioxide (CO2) emission rates from sedentary subjects performing light work on tablets or smartphones in controlled chamber exposures. Five groups, each consisting of four people (four groups with two females and two males and one with three males and one female), stayed in a 22.5 m3 stainless steel chamber under different environmental conditions for 3 h in the morning and then 2,5 h in the afternoon after having a light lunch. Three groups consisted of young adults (college students), one of seniors, and one of teenagers. The chamber was ventilated with outdoor air at 3.2 h−1 (per person rate was 5 L/s). The CO2 emission rates per person were calculated using a single-zone mass-balance equation and the measured CO2 concentration once steady state had been reached. Per person emission rates varied between 14.1 and 16.8 L/h in the morning and 15.9–17.8 L/h in the afternoon; higher levels in the afternoon were probably caused by the increased metabolism from diet-induced thermogenesis (DIT). Emission rates were higher with increased temperature when the participants felt warm, but did not change with increased relative humidity or ozone concentration. They differed to some extent from those estimated using ISO 8996 and ASTM DS 6245, but were similar to published measured CO2 emission rates. The present results require confirmation with more people and measurements of CO2 emission rates using the calorimetric method.

Metabolic Response to Daytime Dry Fasting in Bahá’í Volunteers—Results of a Preliminary Study

Each year in March, adherents of the Bahá’í faith abstain from eating and drinking from sunrise to sunset for 19 days. Thus, Bahá’í fasting (BF) can be considered as a form of daytime dry fasting. We investigated whether BF decreased energy expenditure after a meal and whether it improved anthropometric measures and systemic and tissue-level metabolic parameters. This was a self-controlled cohort study with 11 healthy men. We measured anthropometric parameters, metabolic markers in venous blood and pre- and postprandial energy metabolism at systemic (indirect calorimetry) and tissue (adipose tissue and skeletal muscle microdialysis) level, both before and during BF. During BF, we found reduced body weight, body mass index, body fat and blood glucose. Postprandial increase in energy expenditure was lower and diet-induced thermogenesis tended to be lower as well. In adipose tissue, perfusion, glucose supply and lipolysis were increased. In skeletal muscle, tissue perfusion did not change. Glucose supply and lipolysis were decreased. Glucose oxidation was increased, indicating improved insulin sensitivity. BF may be a promising approach to losing weight and improving metabolism and health. However, outside the context of religiously motivated fasting, skipping a meal in the evening (dinner cancelling) might be recommended, as metabolism appeared to be reduced in the evening.

Targeting PLD2 in adipocytes augments adaptive thermogenesis by improving mitochondrial quality and quantity in mice.

Phospholipase D (PLD)2 via its enzymatic activity regulates cell proliferation and migration and thus is implicated in cancer. However, the role of PLD2 in obesity and type 2 diabetes has not previously been investigated. Here, we show that during diet-induced thermogenesis and obesity, levels of PLD2 but not PLD1 in adipose tissue are inversely related with uncoupling protein 1, a key thermogenic protein. We demonstrate that the thermogenic program in adipose tissue is significantly augmented in mice with adipocyte-specific Pld2 deletion or treated with a PLD2-specific inhibitor and that these mice are resistant to high fat diet-induced obesity, glucose intolerance, and insulin resistance. Mechanistically, we show that Pld2 deletion in adipose tissue or PLD2 pharmacoinhibition acts via p62 to improve mitochondrial quality and quantity in adipocytes. Thus, PLD2 inhibition is an attractive therapeutic approach for obesity and type 2 diabetes by resolving defects in diet-induced thermogenesis.

How much does it cost? Teaching physiology of energy metabolism in mice using an indirect calorimetry system in a practical course for veterinary students.

In endothermic mammals total energy expenditure (EE) is composed of basal metabolic rate (BMR), energy spent for muscle activity, thermoregulation, any kind of production (such as milk, meat, or egg production), and the thermic effect of feeding. The BMR is predominantly determined by body mass and the surface-to-volume ratio of the body. The EE can be quantified by either direct or indirect calorimetry. Direct calorimetry measures the rate of heat loss from the body, whereas indirect calorimetry measures oxygen consumption and carbon dioxide production and calculates heat production from oxidative nutrient combustion. A deep and sustainable understanding of EE in animals is crucial for veterinarians to properly calculate and evaluate feed rations during special circumstances such as anesthesia or in situations with increased energy demands as commonly seen in high-yielding livestock. The practical class described in this article provides an experimental approach to understanding how EE can be measured and calculated by indirect calorimetry. Two important factors that affect the EE of animals (the thermic effect of feeding and the effect of ambient temperature) are measured. A profound knowledge about the energy requirements of animal life and its measurement is also relevant for education in general biology, animal and human physiology, and nutrition. Therefore, this teaching unit can equally well be implemented in other areas of life sciences.

Chewing increases postprandial diet-induced thermogenesis

Slow eating, which involves chewing food slowly and thoroughly, is an effective strategy for controlling appetite in order to avoid being overweight or obese. Slow eating also has the effect of increasing postprandial energy expenditure (diet-induced thermogenesis). It is still unclear whether this is due to oral stimuli; that is, the duration of tasting food in the mouth and the duration of chewing. To investigate the effects of oral stimuli on diet-induced thermogenesis in 11 healthy normal weight males, we conducted a randomized crossover study comprising three trials: (1) drinking liquid food normally, (2) drinking liquid food after tasting, and (3) adding chewing while tasting. Oral stimuli (i.e., the duration of tasting liquid food in the mouth and the duration of chewing) significantly increased diet-induced thermogenesis after drinking liquid food. This result demonstrates that the increase in diet-induced thermogenesis is due to oral stimuli rather than the influence of the food bolus. Increased diet-induced thermogenesis induced by chewing and taste stimuli may help to prevent overweight and obesity.

Mechanisms of obesity in children and adults with phenylketonuria on contemporary treatment.

Obesity prevalence in people with phenylketonuria (PKU) is comparable to that of the general population but the underlying aetiology remains unknown. To assess body composition, dietary intake, moderate physical activity duration (MPAD) and energy expenditure (MPAEE), resting metabolic rate (RMR), diet-induced thermogenesis (DIT), fasting and postprandial fat (FOx) and carbohydrate oxidation (CHOOx), in PKU people and healthy Controls. Participants were PKU people (n=16) and healthy controls (n=15). Body composition was measured with stable isotopes using deuterium as tracer, dietary intake from 4-day food diaries, MPAD and MPAEE from 7-day activity counts measured by triaxial accelerometers, calibrated against individual rates of oxygen consumption and carbon dioxide production, RMR, DIT, FOx and CHOOx by indirect calorimetry. Body composition, DIT, FOx, CHOOx and RMR did not differ between the PKU and the Control groups. MPAD (PKU, 73±26min/week; Control, 152±43min/week) and MPAEE (PKU, 404±127kcal/week; Control, 741±153kcal/week) were lower (P<0.05) in the PKU than the Control group. Raised phenylalanine levels were inversely related with MPAD and MPAEE. Energy intake and energy provided by protein did not differ between the groups, while energy proportion obtained from carbohydrate was higher (PKU, 60±2%; Control, 51±2%; P<0.05) and from fat lower (PKU, 24±2%; Control, 35±3%; P<0.05) in the PKU than in the Control group. People with PKU spent less time and expend less energy in moderate physical activity and have a higher intake of energy from CHO which may be involved in the underlying mechanisms of obesity in PKU.

Pecan-enriched diets increase energy expenditure and fat oxidation in adults at-risk for cardiovascular disease in a randomised, controlled trial.

Research indicates that diets enriched with unsaturated fatty acids improve energy metabolism, although studies on tree nuts, which are a rich source of those fats, are limited. The present study aimed to examine the impact of daily pecan consumption for 8 weeks on energy metabolism in adults with hypercholesterolaemia or at higher risk for cardiovascular disease (CVD) (body mass index ≥ 28 kgm-2 ). For this randomised, controlled trial, 56 sedentary adults were randomised into one of three treatments for an 8-week intervention: two pecan groups and a nut-free control group (n = 18). The ADD group (n = 16) consumed pecans as part of a free-living diet, whereas the SUB group (n = 18) substituted the pecans for isocaloric foods from their habitual diet. At baseline and 8 weeks, a high saturated fat meal was consumed along with indirect calorimetry measurements at fasting and for 4 h postprandially to determine changes in resting metabolic rate (RMR), diet induced thermogenesis (DIT) and substrate utilisation (primary outcomes). Forty-seven participants completed the trial and were included in analyses. In the SUB group, there was an increase in fasting RMR (1607 ± 117 to 1701 ± 114 kcalday-1 ; p = 0.01) and fasting fat oxidation (0.83 ± 0.08 to 0.99 ± 0.08 g/15 min; p = 0.009) and a decrease in fasting respiratory exchange ratio (0.85 ± 0.01 to 0.83 ± 0.01; p = 0.05) from pre- to post-intervention. In the ADD group, there was an increase in postprandial DIT (p < 0.001). There were no changes within the control group or between groups for any outcome measure. Daily consumption of pecans may increase select measures of energy expenditure and fat oxidation in adults at-risk for CVD.

Epigenetic interaction between UTX and DNMT1 regulates diet-induced myogenic remodeling in brown fat

Brown adipocytes share the same developmental origin with skeletal muscle. Here we find that a brown adipocyte-to-myocyte remodeling also exists in mature brown adipocytes, and is induced by prolonged high fat diet (HFD) feeding, leading to brown fat dysfunction. This process is regulated by the interaction of epigenetic pathways involving histone and DNA methylation. In mature brown adipocytes, the histone demethylase UTX maintains persistent demethylation of the repressive mark H3K27me3 at Prdm16 promoter, leading to high Prdm16 expression. PRDM16 then recruits DNA methyltransferase DNMT1 to Myod1 promoter, causing Myod1 promoter hypermethylation and suppressing its expression. The interaction between PRDM16 and DNMT1 coordinately serves to maintain brown adipocyte identity while repressing myogenic remodeling in mature brown adipocytes, thus promoting their active brown adipocyte thermogenic function. Suppressing this interaction by HFD feeding induces brown adipocyte-to-myocyte remodeling, which limits brown adipocyte thermogenic capacity and compromises diet-induced thermogenesis, leading to the development of obesity.