Muscle Energy Metabolism Research Articles

MODELING AND SIMULATION OF SKELETAL MUSCLE BASED ON METABOLISM PHYSIOLOGY

Skeletal muscle energy metabolism plays a very important role in controlling movement of the whole body and has important theoretical guidance for making exercise training plans and losing weight. In this paper, we developed a mathematical model of skeletal muscle excitation–contraction pathway based on the energy metabolism that links excitation to contraction to explore the effects of different metabolic energy systems on calcium ion changes and the force during skeletal muscle contraction. In this paper, a membrane potential model, a calcium cycle model, a cross-bridge dynamics model and an energy metabolism model were established. Finally, the physiological phenomenon of calcium ion transport and calcium ion concentration change of the sarcoplasm was simulated. The results show that the phosphagen system has the fastest metabolic rate and the phosphagen system has the largest impact on the explosive power of skeletal muscle exercise. The specific characteristics of the three metabolic energy systems supporting skeletal muscle movement in vivo were also analyzed in detail.

Search for proteomic markers for stunning stress and stress-induced textural tenderization in silver carp (Hypophthalmichthys molitrix) fillets using label-free strategy

A differential proteome analysis using label-free strategy was conducted to elucidate the stunning stress-induced proteome changes and its relationship to textural softening in silver carp (Hypophthalmichthys molitrix) fillets. Compared with the muscle proteome of fillets stunned by percussion, ice/water and gill cut stunning resulted in 43 differentially abundant proteins (DAPs) that were involved in muscle contraction, energy metabolism, antioxidant defense, protein turnover, etc., and gill cut-stunned fillets showed the most significant proteome changes with 28 up- and down-regulated DAPs. In addition, textural softening was more obvious in ice/water- and gill cut-treated fillets and was closely correlated to 21 DAPs including fast muscle troponin T, fragments of myosin, superoxide dismutase [Cu-Zn], ribosomal protein L38, isoform 2 of heat shock cognate 70, two subunits of proteasome, etc., and those DAPs were selected as potential proteomic markers to trace the accelerated textural softening in stunning-stressed fillets.

Simvastatin Impairs Glucose Homeostasis in Mice Depending on PGC-1α Skeletal Muscle Expression.

Several studies showed an increased risk for diabetes with statin treatment. PGC-1α is an important regulator of muscle energy metabolism and mitochondrial biogenesis. Since statins impair skeletal muscle PGC-1α expression and reduced PGC-1α expression has been observed in diabetic patients, we investigated the possibility that skeletal muscle PGC1α expression influences the effect of simvastatin on muscle glucose metabolism. Mice with muscle PGC-1α knockout (KO) or PGC-1α overexpression (OE), and wild-type (WT) mice were investigated. Mice were treated orally for 3 weeks with simvastatin (5 mg/kg/day) and investigated by intraperitoneal glucose tolerance (iGTT), in vivo skeletal muscle glucose uptake, muscle glycogen content, and Glut4 and hexokinase mRNA and protein expression. Simvastatin impaired glucose metabolism in WT mice, as manifested by increased glucose blood concentrations during the iGTT, decreased skeletal muscle glucose uptake and glycogen stores. KO mice showed impaired glucose homeostasis with increased blood glucose concentrations during the iGTT already without simvastatin treatment and simvastatin induced a decrease in skeletal muscle glucose uptake. In OE mice, simvastatin treatment increased blood glucose and insulin concentrations during the iGTT, and increased skeletal muscle glucose uptake, glycogen stores, and Glut4 and hexokinase protein expression. In conclusion, simvastatin impaired skeletal muscle insulin sensitivity in WT mice, while KO mice exhibited impaired skeletal muscle insulin sensitivity already in the absence of simvastatin. In OE mice, simvastatin augmented muscular glucose uptake but impaired whole-body insulin sensitivity. Thus, simvastatin affected glucose homeostasis depending on PGC-1α expression.

Substrate oxidation in primary human skeletal muscle cells is influenced by donor age

Primary human myotubes represent an alternative system to intact skeletal muscle for the study of human diseases related to changes in muscle energy metabolism. This work aimed to study if fatty acid and glucose metabolism in human myotubes in vitro were related to muscle of origin, donor gender, age, or body mass index (BMI). Myotubes from a total of 82 donors were established from three different skeletal muscles, i.e., musculus vastus lateralis, musculus obliquus internus abdominis, and musculi interspinales, and cellular energy metabolism was evaluated. Multiple linear regression analyses showed that donor age had a significant effect on glucose and oleic acid oxidation after correcting for gender, BMI, and muscle of origin. Donor BMI was the only significant contributor to cellular oleic acid uptake, whereas cellular glucose uptake did not rely on any of the variables examined. Despite the effect of age on substrate oxidation, cellular mRNA expression of pyruvate dehydrogenase kinase 4 (PDK4) and peroxisome proliferator–activated receptor gamma coactivator 1 alpha (PPARGC1A) did not correlate with donor age. In conclusion, donor age significantly impacts substrate oxidation in cultured human myotubes, whereas donor BMI affects cellular oleic acid uptake.

Author Correction: Skeletal muscle energy metabolism during exercise.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Zinc-α2-glycoprotein promotes skeletal muscle lipid metabolism in cold-stressed mice.

Skeletal muscle is the most abundant tissue in the adult body and plays an essential role in maintaining heat production for the entire body. Recently, muscle-derived non-shivering thermogenesis under cold conditions has received much attention. Zinc-α2-glycoprotein (ZAG) is an adipokine that was shown to influence energy metabolism in the adipose tissue. We used ZAG knock-out (ZAG KO) and wild-type (WT) mice to investigate the effect of ZAG on the lipid metabolism of skeletal muscle upon exposure to a low temperature (6°C) for one week. The results show that cold stress significantly increases the level of lipolysis, energy metabolism, and fat browning-related proteins in the gastrocnemius muscle of WT mice. In contrast, ZAG KO mice did not show any corresponding changes. Increased expression of β3-adrenoceptor (β3-AR) and protein kinase A (PKA) might be involved in the ZAG pathway in mice exposed cold stress. Furthermore, expression of lipolysis-related proteins (ATGL and p-HSL) and energy metabolism-related protein (PGC1α, UCP2, UCP3 and COX1) was significantly enhanced in ZAG KO mice after injection of ZAG-recombinant plasmids. These results indicate that ZAG promotes lipid-related metabolism in the skeletal muscle when the animals are exposed to low temperatures. This finding provides a promising target for the development of new therapeutic approaches to improve skeletal muscle energy metabolism.

Impact of aerobic exercise type on blood flow, muscle energy metabolism, and mitochondrial biogenesis in experimental lower extremity artery disease

Exercise training (ET) is recommended for lower extremity artery disease (LEAD) management. However, there is still little information on the hemodynamic and metabolic adaptations by skeletal muscle with ET. We examined whether hindlimb perfusion/vascularization and muscle energy metabolism are altered differently by three types of aerobic ET. ApoE−/− mice with LEAD were assigned to one of four groups for 4 weeks: sedentary (SED), forced treadmill running (FTR), voluntary wheel running (VWR), or forced swimming (FS). Voluntary exercise capacity was improved and equally as efficient with FTR and VWR, but remained unchanged with FS. Neither ischemic hindlimb perfusion and oxygenation, nor arteriolar density and mRNA expression of arteriogenic-related genes differed between groups. 18FDG PET imaging revealed no difference in the steady-state levels of phosphorylated 18FDG in ischemic and non-ischemic hindlimb muscle between groups, nor was glycogen content or mRNA and protein expression of glucose metabolism-related genes in ischemic muscle modified. mRNA (but not protein) expression of lipid metabolism-related genes was upregulated across all exercise groups, particularly by non-ischemic muscle. Markers of mitochondrial content (mitochondrial DNA content and citrate synthase activity) as well as mRNA expression of mitochondrial biogenesis-related genes in muscle were not increased with ET. Contrary to FTR and VWR, swimming was ineffective in improving voluntary exercise capacity. The underlying hindlimb hemodynamics or muscle energy metabolism are unable to explain the benefits of running exercise.

Transcriptional Changes Involved in Atrophying Muscles during Prolonged Fasting in Rats.

Food deprivation resulting in muscle atrophy may be detrimental to health. To better understand how muscle mass is regulated during such a nutritional challenge, the current study deciphered muscle responses during phase 2 (P2, protein sparing) and phase 3 (P3, protein mobilization) of prolonged fasting in rats. This was done using transcriptomics analysis and a series of biochemistry measurements. The main findings highlight changes for plasma catabolic and anabolic stimuli, as well as for muscle transcriptome, energy metabolism, and oxidative stress. Changes were generally consistent with the intense use of lipids as fuels during P2. They also reflected increased muscle protein degradation and repressed synthesis, in a more marked manner during P3 than P2 compared to the fed state. Nevertheless, several unexpected changes appeared to be in favor of muscle protein synthesis during fasting, notably at the level of the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway, transcription and translation processes, and the response to oxidative stress. Such mechanisms might promote protein sparing during P2 and prepare the restoration of the protein compartment during P3 in anticipation of food intake for optimizing the effects of an upcoming refeeding, thereby promoting body maintenance and survival. Future studies should examine relevance of such targets for improving nitrogen balance during catabolic diseases.

Overexpression of AMPD2 indicates poor prognosis in colorectal cancer patients via the Notch3 signaling pathway.

BACKGROUNDAMPD2 is a critical enzyme catalyzing smooth muscle energy supply and metabolism; however, its cellular biological function and clinical implication in colorectal cancer (CRC) are largely unknown.AIMTo clarify the role of AMPD2 in CRC and study the pathway and prognostic value of its role.METHODSAMPD2 expression was analyzed by integrated bioinformatics analysis based on TCGA data sets and immunohistochemistry in tissue microarrays, and the correlation between AMPD2 expression and clinicopathological parameters, Notch3 expression, and prognostic features was assessed. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis were then performed to investigate the regulatory pathway involved. The effects of AMPD2 expression on CRC cells and Notch3 protein expression were investigated by downregulation and overexpression of AMPD2.RESULTSAMPD2 mRNA was significantly overexpressed in tumor tissue when compared with normal tissue in a cohort of the TCGA-COAD data set. Biological function enrichment analysis indicated that the Notch pathway strongly correlated with AMPD2 expression, and that the expression of Notch3 and JAG2 mRNA was positively associated with AMPD2 in CRC tissues. In vitro, AMPD2 overexpression markedly reduced Notch3 protein expression in CRC cells, while knockdown of AMPD2 showed the opposite findings. In addition, protein expression was significantly up-regulated in our CRC cohort as indicated by tissue microarray analysis. High expression of AMPD2 protein correlated with advanced depth of tumor and poor differentiation. Furthermore, high AMPD2 expression in CRC tissues was an indicator of poor outcome for CRC patients.CONCLUSIONAMPD2 is commonly overexpressed in CRC, and acts as a metabolism oncogene to induce CRC progression through the Notch signaling pathway. Thus, AMPD2 may be a novel prognostic biomarker for CRC.

Skeletal muscle energy metabolism during exercise.

The continual supply of ATP to the fundamental cellular processes that underpin skeletal muscle contraction during exercise is essential for sports performance in events lasting seconds to several hours. Because the muscle stores of ATP are small, metabolic pathways must be activated to maintain the required rates of ATP resynthesis. These pathways include phosphocreatine and muscle glycogen breakdown, thus enabling substrate-level phosphorylation ('anaerobic') and oxidative phosphorylation by using reducing equivalents from carbohydrate and fat metabolism ('aerobic'). The relative contribution of these metabolic pathways is primarily determined by the intensity and duration of exercise. For most events at the Olympics, carbohydrate is the primary fuel for anaerobic and aerobic metabolism. Here, we provide an overview of exercise metabolism and the key regulatory mechanisms ensuring that ATP resynthesis is closely matched to the ATP demand of exercise. We also summarize various interventions that target muscle metabolism for ergogenic benefit in athletic events.

Day-night rhythm of skeletal muscle metabolism is disturbed in older, metabolically compromised individuals

ObjectiveSkeletal muscle mitochondrial function and energy metabolism displays day-night rhythmicity in healthy, young individuals. Twenty-four-hour rhythmicity of metabolism has been implicated in the etiology of age-related metabolic disorders. Whether day-night rhythmicity in skeletal muscle mitochondrial function and energy metabolism is altered in older, metabolically comprised humans remains unknown. MethodsTwelve male overweight volunteers with impaired glucose tolerance and insulin sensitivity stayed in a metabolic research unit for 2 days under free living conditions with regular meals. Indirect calorimetry was performed at 5 time points (8 AM, 1 PM, 6 PM, 11 PM, 4 AM), followed by a muscle biopsy. Mitochondrial oxidative capacity was measured in permeabilized muscle fibers using high-resolution respirometry. ResultsMitochondrial oxidative capacity did not display rhythmicity. The expression of circadian core clock genes BMAL1 and REV-ERBα showed a clear day-night rhythm (p < 0.001), peaking at the end of the waking period. Remarkably, the repressor clock gene PER2 did not show rhythmicity, whereas PER1 and PER3 were strongly rhythmic (p < 0.001). On the whole-body level, resting energy expenditure was highest in the late evening (p < 0.001). Respiratory exchange ratio did not decrease during the night, indicating metabolic inflexibility. ConclusionsMitochondrial oxidative capacity does not show a day-night rhythm in older, overweight participants with impaired glucose tolerance and insulin sensitivity. In addition, gene expression of PER2 in skeletal muscle indicates that rhythmicity of the negative feedback loop of the molecular clock is disturbed. ClinicalTrials.gov IDNCT03733743.

Skeletal muscle dysregulation in rheumatoid arthritis: Metabolic and molecular markers in a rodent model and patients.

Rheumatoid arthritis (RA) is accompanied by pain, inflammation and muscle weakness. Skeletal muscle inflammation and inactivity are independently associated with muscle insulin resistance and atrophy. Our objective was to identify early molecular and biochemical markers in muscle from a rodent model of RA relative to control and subsequently identify commonality in muscle gene expression between this model and muscle from RA patients. Pain behaviour and locomotor activity were measured in a collagen-induced arthritis (CIA) model of RA (n = 9) and control (n = 9) rats. Energy substrates and metabolites, total alkaline-soluble protein:DNA ratio and mRNA abundance of 46 targeted genes were also determined in Extensor digitorum longus muscle. Expression of targeted mRNAs was quantified in Vastus Lateralis muscle from RA patients (n = 7) and healthy age-matched control volunteers (n = 6). CIA rats exhibited pain behaviour (p<0.01) and reduced activity (p<0.05) compared to controls. Muscle glycogen content was less (p<0.05) and muscle lactate content greater (p<0.01) in CIA rats. The bioinformatics analysis of muscle mRNA abundance differences from the control, predicted the activation of muscle protein metabolism and inhibition of muscle carbohydrate and fatty acid metabolism in CIA rats. Compared to age-matched control volunteers, RA patients exhibited altered muscle mRNA expression of 8 of the transcripts included as targets in the CIA model of RA. In conclusion, muscle energy metabolism and metabolic gene expression were altered in the CIA model, which was partly corroborated by targeted muscle mRNA measurements in RA patients. This research highlights the negative impact of RA on skeletal muscle metabolic homeostasis.

Self-Eating for Muscle Fitness: Autophagy in the Control of Energy Metabolism.

Cellular processes that sense and transmit metabolic changes are crucial for adaptation to external signals. In this regard, autophagy provides energy upon nutrient deprivation and represents a quality control mechanism that eliminates damaged organelles or proteins. Here, we review recent findings on the metabolic pathways controlling autophagy in skeletal muscle, a plastic tissue that undergoes major changes in energy demands. We also analyze the implications of autophagy in the regulation of energy metabolism in muscle and how alterations in this process affect energy homeostasis at the whole-body level and the development of metabolic diseases and aging.

Polyphenols: Potential Beneficial Effects of These Phytochemicals in Athletes.

An athlete's dietary requirements depend on several aspects, including the environment, the sport, and the athlete's goals. Although it is recognized that regular exercise improves muscle performance and energy metabolism, unaccustomed or excessive exercise may cause cell damage and impair muscle function by triggering tissue inflammation and oxidative stress. Supplement use among athletes is widespread and recently new attention has been applied to polyphenols. Polyphenols are a class of organic chemical compounds, mainly found in plants, characterized by the presence of multiples of phenol structural units, and over recent decades, special attention has been paid to the healthy role of fruit-derived polyphenols in the human diet. This article will summarize latest knowledge on polyphenolic compounds that have been demonstrated both to exert an effect in exercise-induced muscle damage and to play a biological/physiological role in improving physical performance.

Skeletal Muscle Metabolic Gene Profile Associates With Rheumatoid Arthritis Improvements Following High Intensity Interval Training

Rheumatoid arthritis (RA) is a systemic inflammatory disease characterized by exercise intolerance and increased risk for cardiometabolic disease. High intensity interval training (HIIT) improves both inflammation and cardiorespiratory fitness (CRF) in RA, however the mechanisms underpinning these therapeutic benefits are unclear. PURPOSE: To identify baseline skeletal muscle pathways linking HIIT with improvements in RA inflammatory disease activity and CRF. METHODS: Participants with RA (n=13; mean age=63.9±7.2) underwent RA disease activity (DAS), physiologic, and biologic assessments pre- and post-10 weeks of supervised HIIT. Cardiopulmonary exercise testing measured CRF as rVO2 peak (mL/kg/min). Skeletal muscle RNA was isolated from vastus lateralis biopsies. Illumina Human HT-12v4 Expression BeadChips and Ingenuity Pathway Analysis were used for quantitative whole genome RNA analyses. Differential Spearman correlations (p<0.05) assessed associations for baseline gene expression with ΔDAS and ΔCRF (post - pre). RESULTS: HIIT improved RA DAS (+23.8%; p<0.001) and CRF (+8.2%; p<0.001). ΔDAS was strongly correlated with baseline muscle expression of 46 genes (0.80< r<-0.80; *p<0.001); including genes encoding proteins involved in substrate energy metabolism (n=9; LIAS, NDUFV3, GLDC, AGL, BCKDHB, PDK2, LDHB, ACSS2, PANK2) and inflammatory pathways (n=4; FCRL6, TNFRSF19, CMTM4, NKG7). In contrast, ΔCRF was strongly correlated with baseline expression of 16 genes; only 1 (NDUFB4) involved in cellular metabolism and 0 in inflammation. Novel network analysis revealed muscle upregulation of NF-kB and MAPK/JNK pathways associated with greater improvements in DAS. CONCLUSIONS: HIIT-mediated improvements in RA disease activity associate strongly with baseline alterations in skeletal muscle metabolic and inflammatory pathways. Thus, exercise training may improve RA inflammation via coordinated regulation of muscle and immune cell energy metabolism.

Muscle oxygenation, endocrine and metabolic regulation during low-intensity endurance exercise with blood flow restriction.

[Purpose]The present study investigated the effect of endurance exercise with blood flow restriction (BFR) performed at either 25% maximal oxygen uptake ( max) or 40% max) on muscle oxygenation, energy metabolism, and endocrine responses.[Methods]Ten males were recruited in the present study. The subjects performed three trials: (1) endurance exercise at 40% max without BFR (NBFR40), (2) endurance exercise at 25% max with BFR (BFR25), and (3) endurance exercise at 40% max with BFR (BFR40). The exercises were performed for 15 min during which the pedaling frequency was set at 70 rpm. In BFR25 and BFR40, 2 min of pressure phase (equivalent to 160 mmHg) followed by 1 min of release phase were repeated five times (5 × 3 min) throughout 15 minutes of exercise. During exercise, muscle oxygenation and concentration of respiratory gases were measured. The blood samples were collected before exercise, immediately after 15 min of exercise, and at 15, 30, and 60 minutes after completion of exercise.[Results]Deoxygenated hemoglobin (deoxy-Hb) level during exercise was significantly higher with BFR25 and BFR40 than that with NBFR40. BFR40 showed significantly higher total-hemoglobin (total-Hb) than NBFR40 during 2 min of pressure phase. Moreover, exercise-induced lactate elevation and pH reduction were significantly augmented in BFR40, with concomitant increase in serum cortisol concentration after exercise. Carbohydrate (CHO) oxidation was significantly higher with BFR40 than that with NBFR40 and BFR25, whereas fat oxidation was lower with BFR40.[Conclusion]Deoxy-Hb and total Hb levels were significantly increased during 15 min of pedaling exercise in BFR25 and BFR40, indicating augmented local hypoxia and blood volume (blood perfusion) in the muscle. Moreover, low-and moderate-intensity exercise with BFR facilitated CHO oxidation.

Multinuclear MRS at 7T Uncovers Exercise Driven Differences in Skeletal Muscle Energy Metabolism Between Young and Seniors.

Purpose: Aging is associated with changes in muscle energy metabolism. Proton (1H) and phosphorous (31P) magnetic resonance spectroscopy (MRS) has been successfully applied for non-invasive investigation of skeletal muscle metabolism. The aim of this study was to detect differences in adenosine triphosphate (ATP) production in the aging muscle by 31P-MRS and to identify potential changes associated with buffer capacity of muscle carnosine by 1H-MRS.Methods: Fifteen young and nineteen elderly volunteers were examined. 1H and 31P-MRS spectra were acquired at high field (7T). The investigation included carnosine quantification using 1H-MRS and resting and dynamic 31P-MRS, both including saturation transfer measurements of phosphocreatine (PCr), and inorganic phosphate (Pi)-to-ATP metabolic fluxes.Results: Elderly volunteers had higher time constant of PCr recovery (τPCr) in comparison to the young volunteers. Exercise was connected with significant decrease in PCr-to-ATP flux in both groups. Moreover, PCr-to-ATP flux was significantly higher in young compared to elderly both at rest and during exercise. Similarly, an increment of Pi-to-ATP flux with exercise was found in both groups but the intergroup difference was only observed during exercise. Elderly had lower muscle carnosine concentration and lower postexercise pH. A strong increase in phosphomonoester (PME) concentration was observed with exercise in elderly, and a faster Pi:PCr kinetics was found in young volunteers compared to elderly during the recovery period.Conclusion: Observations of a massive increment of PME concentration together with high Pi-to-ATP flux during exercise in seniors refer to decreased ability of the muscle to meet the metabolic requirements of exercise and thus a limited ability of seniors to effectively support the exercise load.

Acetylation and Phosphorylation of Proteins Affect Energy Metabolism and Pork Quality.

Preslaughter handling has been shown to significantly affect meat quality, but the mechanisms are not fully understood. In this study, we investigated protein phosphorylation and acetylation in pig muscles at early postmortem time and their associations with meat quality attributes. Thirty pigs were randomly assigned to traditional (TH, n = 15) or mild handling (MH, n = 15). Compared with TH, MH reduced the incidence of pale, soft, and exudative (PSE) or dark, firm, and dry (DFD) pork. MH induced 65 and 20 peptides that match with 39 and 12 proteins to be more highly phosphorylated and acetylated, respectively. Creatine kinase, β-enolase, α-1,4-glucan phosphorylase, tropomyosin, and myosin heavy chain isoforms 1, 4, and 7 were found to be simultaneously phosphorylated and acetylated, which may involve glycolysis, tight junctions, and muscle contraction. The phosphorylation and acetylation levels of differential proteins showed significant correlations with meat quality traits. These findings indicate that preslaughter MH can improve meat quality by regulating protein phosphorylation and acetylation involving energy metabolism in muscle.

BDNF as a novel therapeutic candidate for Kennedy's disease.

BDNF as a novel therapeutic candidate for Kennedy's disease.

Taurine Stimulates Thermoregulatory Genes in Brown Fat Tissue and Muscle without an Influence on Inguinal White Fat Tissue in a High-Fat Diet-Induced Obese Mouse Model.

This study was conducted to investigate if taurine supplementation stimulates the induction of thermogenic genes in fat tissues and muscles and decipher the mechanism by which taurine exerts its anti-obesity effect in a mildly obese ICR (CD-1®) mouse model. Three groups of ICR mice were fed a normal chow diet, a high-fat diet (HFD), or HFD supplemented with 2% taurine in drinking water for 28 weeks. The expression profiles of various genes were analyzed by real time PCR in interscapular brown adipose tissue (BAT), inguinal white adipose tissue (iWAT), and the quadriceps muscles of the experimental groups. Genes that are known to regulate thermogenesis like PGC-1α, UCP-1, Cox7a1, Cox8b, CIDE-A, and β1-, β2-, and β3-adrenergic receptors (β-ARs) were found to be differentially expressed in the three tissues. These genes were expressed at a very low level in iWAT as compared to BAT and muscle. Whereas, HFD increased the expression of these genes. Taurine supplementation stimulated the expression of UCP-1, Cox7a1, and Cox8b in BAT and only Cox7a1 in muscle, while there was a decrease in iWAT. In contrast, fat deposition-related genes, monoamine oxidases (MAO)-A, and -B, and lipin-1, were decreased by taurine supplementation only in iWAT and not in BAT or muscle. In conclusion, the potential anti-obesity effects of taurine may be partly due to upregulated thermogenesis in BAT, energy metabolism of muscle, and downregulated fat deposition in iWAT.