Nicotinamide Riboside (NR) is a NAD+ booster with wide physiological repercussion including the improvement on glucose and lipid homeostasis, increasing the life expectancy in mammals. However, the ...effects of NR on metabolism are only partially known. Here, we evaluated the effects of NR on the thermogenic response, highlighting the brown adipose tissue (BAT) in lean mice.
Male C57BL/67 mice were supplement with NR (400 mg/Kg/day) during 5 weeks. The Comprehensive Lab Animal Monitoring System (CLAMS) and thermographic images were used to evaluated the physiological effects of NR treatment. The BAT were extracted and analyzed by Western Blotting and qPCR. Also, bioinformatics analyses were performed to establish the connection between the NAD+ synthesis pathway in BAT and thermogenic response in several isogenic strains of BXD mice.
Transcriptomic analysis revealed that genes involved in NAD+ synthesis (Nampt and Nmnat1) in the BAT were negatively correlated with body weight and fat mass. The heat map showed a strong positive correlation between Nampt and Ucp1 mRNA in BAT and body temperature in several strains of BXD lean mice. The experimental approaches demonstrated that oral NR supplementation reduced the abdominal visceral fat depots, with discrete impact on oxygen consumption in C57BL/6J mice. Interestingly, NR significantly increased the body temperature, and this phenomenon was accompanied by high levels of UCP1 protein content and Pgc1α mRNA in BAT.
This study demonstrated the oral NR supplementation was sufficient to induce the thermogenic response in lean mice changing the BAT metabolism.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
Strontium titanate nanoparticles have attracted much attention due to their physical and chemical properties, especially as photocatalysts under ultraviolet irradiation. In this paper, we analyze the ...effect of heating rate during the crystallization process of SrTiO3 nanoparticles in the degradation of organic pollutants. The relationship between structural, morphological and photocatalytic properties of the SrTiO3 nanoparticles was investigated using different techniques. Transmission electron microscopy and N2 adsorption results show that particle size and surface properties are tuned by the heating rate of the SrTiO3 crystallization process. The SrTiO3 nanoparticles showed good photoactivity for the degradation of methylene blue, rhodamine B and methyl orange dyes, driven by a nonselective process. The SrTiO3 sample with the largest particle size exhibited higher photoactivity per unit area, independent of the molecule to be degraded. The results pointed out that the photodegradation of methylene blue dye catalyzed by SrTiO3 is caused by the action of valence band holes (direct pathway), and the indirect mechanism has a negligible effect, i.e. degradation by O2−• and •OH radicals attack.
Strontium titanate (SrTiO3) nanoparticles have attracted much attention due to their physical and chemical properties, especially as photocatalysts under UV irradiation. SrTiO3 nanospheres were obtained by polymeric precursor method and evaluated on the degradation of organic pollutants. All of the photocatalysts showed a good activity for the photodegradation of methylene blue, rhodamine B and methyl orange dyes, driven by a nonselective process. The SrTiO3 sample with the largest particle size exhibited a higher photoactivity per unit area, independent of the molecule to be degraded. The photodegradation of MB dye catalyzed by SrTiO3 is caused by the action of valence band holes.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Abstract
The impairment of the mitochondrial functions is a hallmark of aging. During aging, there is a downregulation of two mechanisms strictly associated with mitochondrial integrity, including ...the mitonuclear imbalance (eg, imbalance in mitochondrial- versus nuclear-encoded mitochondrial proteins) and the mitochondrial unfolded protein response (UPRmt). Here, we evaluated the effects of aerobic exercise in the mitonuclear imbalance and UPRmt markers in the skeletal muscle of old mice. We combined the physiological tests, molecular and bioinformatic analyzes to evaluate the effects of 4 weeks of aerobic exercise training on mitonuclear imbalance and UPRmt markers in the skeletal muscle of young (2 months) and aged (24 months) C57BL/6J mice. Initially, we found that aging reduced several mitochondrial genes in the gastrocnemius muscle, and it was accompanied by the low levels of UPRmt markers, including Yme1l1 and Clpp mRNA. As expected, physical training improved the whole-body metabolism and physical performance of aged mice. The aerobic exercise increased key proteins involved in the mitochondrial biogenesis/functions (VDAC and SIRT1) along with mitochondrial-encoded genes (mtNd1, mtCytB, and mtD-Loop) in the skeletal muscle of old mice. Interestingly, aerobic exercise induced the mitonuclear imbalance, increasing MTCO1/ATP5a ratio and UPRmt markers in the skeletal muscle, including HSP60, Lonp1, and Yme1L1 protein levels in the gastrocnemius muscle of aged mice. These data demonstrate that aerobic exercise training induced mitonuclear imbalance and UPRmt in the skeletal muscle during aging. These phenomena could be involved in the improvement of the mitochondrial metabolism and oxidative capacity in aged individuals.
Sestrins and autophagy deficiencies are associated with several aging-related organic dysfunctions and metabolic disorders. Here we evaluate the effects of acute exercise on Sestrin 2 (Sesn2) protein ...content and autophagy markers in the skeletal muscle of experimental models of aging. Twenty-four months-old C57BL/6J male mice were submitted to a single bout of swimming exercise and the gastrocnemius muscle was evaluated by Western blot. Transcriptomic and phenotypic analysis were also performed by using strains of genetically-diverse BXD mice. The bioinformatics analysis showed a negative correlation between Sesn2 mRNA levels in the skeletal muscle and body weight gain, plasma triglycerides and fasting glucose and positive correlation with several autophagic markers in the muscle of BXD mice. Consistent with these findings, low levels of Sesn2 protein content were observed in the gastrocnemius muscle of C57BL/6J old mice when compared to young group. Interestingly, the acute aerobic exercise induced Sesn2 accumulation and modulated several markers of autophagy in the gastrocnemius muscle old mice, including unc-51-like kinase-1 (Ulk1) phosphorylation and the protein levels of Atg5, Atg7, p62 and LC3-II. Finally, exercise increased insulin sensitivity in old animals, as demonstrated by kITT. Taken together, these findings demonstrated the acutely, aerobic physical exercise recovers Sestrin 2 protein content and induces autophagy in the skeletal muscle of old mice, contributing with the improvement of insulin sensitivity an aging animal model.
•Downregulation of Sestrin2 in the skeletal muscle of old mice.•Exercise stimulates Sestrin2 accumulation in the skeletal muscle of old mice.•Physical exercise elicits autophagy in the skeletal muscle of old mice.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
Galectin-1 is a carbohydrate-binding protein expressed in many tissues. In recent years, increasing evidence has emerged for the role of galectin-1 in obesity, insulin resistance and type 2 diabetes. ...Galectin-1 has been highly conserved through evolution and is involved in key cellular functions such as tissue maturation and homeostasis. It has been shown that galectin-1 increases in obesity, both in the circulation and in the adipose tissue of human and animal models. Several proteomic studies have independently identified an increased galectin-1 expression in the adipose tissue in obesity and in insulin resistance. Large population-based cohorts have demonstrated associations for circulating galectin-1 and markers of insulin resistance and incident type 2 diabetes. Furthermore, galectin-1 is associated with key metabolic pathways including glucose and lipid metabolism, as well as insulin signalling and inflammation. Intervention studies in animal models alter animal weight and metabolic profile. Several studies have also linked galectin-1 to the progression of complications in diabetes, including kidney disease and retinopathy. Here, we review the current knowledge on the clinical potential of galectin-1 in obesity and type 2 diabetes.
Sphingolipids were discovered more than a century ago and were simply considered as a class of cell membrane lipids for a long time. However, after the discovery of several intracellular functions ...and their role in the control of many physiological and pathophysiological conditions, these molecules have gained much attention. For instance, the sphingosine‐1‐phosphate (S1P) is a circulating bioactive sphingolipid capable of triggering strong intracellular reactions through the family of S1P receptors (S1PRs) spread in several cell types and tissues. Recently, the role of S1P in the control of skeletal muscle metabolism, atrophy, regeneration, and metabolic disorders has been widely investigated. In this review, we summarized the knowledge of S1P and its effects in skeletal muscle metabolism, highlighting the role of S1P/S1PRs axis in skeletal muscle regeneration, fatigue, ceramide accumulation, and insulin resistance. Finally, we discussed the physical exercise role in S1P/S1PRs signaling in skeletal muscle cells, and how this nonpharmacological strategy may be prospective for future investigations due to its ability to increase S1P levels.
In the current manuscript, we described the role of sphingolipids, mainly sphingosine‐1‐phosphate (S1P) in skeletal muscle metabolism and functions under a variety of physiological and pathophysiological conditions. Separated by topics, we also discuss the intracellular mechanisms of S1P actions on atrophy, obesity, diabetes and fatigue resistance. Finally, we discussed the role of physical exercise as a therapeutic strategy involving the S1P signaling.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
White adipose tissue (WAT) regulates energy homeostasis by releasing adipokines and modulating cell maintenance. Nutrient excess affects adipocyte hypertrophy directly in WAT by increasing ...excessively the activity of autophagy systems, generating proinflammatory markers and increasing infiltration of macrophages, causing metabolic diseases such as obesity and diabetes. Evidences suggest that cathepsin B (CTSB), a papain-like cysteine peptidase protein, can modulate autophagy processes in adipocytes. This review will focus on the role of CTSB in autophagy under conditions of obesity.
During obese conditions, white adipose tissue (WAT) accumulation causes adipocyte hypertrophy and cathepsin B (CTSB) release, which leads to an excessive increase of autophagy in adipocytes and enhancing of inflammation and macrophage infiltration, therefore contributing to metabolic syndrome. Display omitted
•Cathepsin B (CTSB) modulates autophagy process in adipocytes.•CTSB expression increases during obesity conditions.•CTSB expression modulates inflammatory markers under conditions of obesity.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
Dysfunction of the adipose tissue metabolism is considered as a significant hallmark of aging. It has been proposed that α‐β hydrolase domain containing 5 (ABHD5) plays a critical role in the control ...of lipolysis. However, the role of ABHD5 in the control of lipolysis during aging or exercise is unknown. Here we combined the experimental mouse model with transcriptomic analyzes by using murine and human databases to explore the role of ABHD5 in the adipose tissue during aging and in response to exercise. Transcriptomic data revealed a downregulation of Abhd5 messenger RNA levels in the subcutaneous white adipose tissue (scWAT) over time in individuals from 20 to 69 years old. Aged mice displayed dramatic reduction of ABHD5 protein content and lipolytic‐related proteins in the scWAT. Interestingly, 4 weeks of high‐intensity interval training increased ABHD5 protein level and restored the lipolytic pathway in the scWAT of aged mice. Altogether, our findings demonstrated that aging affects ABHD5 content in the adipose tissue of mice and humans. Conversely, exercise increases ABHD5 activity, recovering the lipolytic activity in aged mice.
Significance statement
Dysfunction of the adipose tissue metabolism is considered as a significant hallmark of aging. Here we identify that a pivotal protein involved in the lipolysis mechanism called α‐β hydrolase domain containing 5 (ABHD5) is downregulated in adipose tissue of aged mice. Conversely, high‐intensity interval training (HIIT) recovered ABHD5 protein content and lipolysis mechanism in the subcutaneous adipose tissue of aged mice.
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FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Hypothalamic sphingosine‐1‐phosphate receptor 1 (S1PR1), the G protein–coupled receptor 1 of sphingosine‐1‐phosphate, has been described as a modulator in the control of energy homeostasis in ...rodents. However, this mechanism is still unclear. Here, we evaluate the role of interleukin 6 (IL‐6) associated with acute physical exercise in the control of the hypothalamic S1PR1–signal transducer and activator of transcription 3 (STAT3) axis. Acute exercise session and an intracerebroventricular IL‐6 injection increased S1PR1 protein content and STAT3 phosphorylation in the hypothalamus of lean and obese mice accompanied by a reduction in food consumption. Transcriptome analysis indicated a strong positive correlation between Il‐6 and S1pr1 messenger RNA in several tissues of genetically diverse BXD mice strains and humans, including in the hypothalamus. Interestingly, exercise failed to stimulate the S1PR1–STAT3 axis in IL‐6 knockout mice and the disruption of hypothalamic‐specific IL‐6 action blocked the anorexigenic effects of exercise. Taken together, our results indicate that physical exercise modulates the S1PR1 protein content in the hypothalamus, through the central action of IL‐6.
Exercise, hypothalamic sphingosine‐1‐phosphate receptor 1, interleukin 6, and hypothalamus.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Hypothalamic inflammation is associated with insulin and leptin resistance, hyperphagia, and obesity. In this scenario, hypothalamic protein tyrosine phosphatase 1B (PTP1B) has emerged as the key ...phosphatase induced by inflammation that is responsible for the central insulin and leptin resistance. Here, we demonstrated that acute exercise reduced inflammation and PTP1B protein level/activity in the hypothalamus of obese rodents. Exercise disrupted the interaction between PTP1B with proteins involved in the early steps of insulin (IRβ and IRS-1) and leptin (JAK2) signaling, increased the tyrosine phosphorylation of these molecules, and restored the anorexigenic effects of insulin and leptin in obese rats. Interestingly, the anti-inflammatory action and the reduction of PTP1B activity mediated by exercise occurred in an interleukin-6 (IL-6)-dependent manner because exercise failed to reduce inflammation and PTP1B protein level after the disruption of hypothalamic-specific IL-6 action in obese rats. Conversely, intracerebroventricular administration of recombinant IL-6 reproduced the effects of exercise, improving hypothalamic insulin and leptin action by reducing the inflammatory signaling and PTP1B activity in obese rats at rest. Taken together, our study reports that physical exercise restores insulin and leptin signaling, at least in part, by reducing hypothalamic PTP1B protein level through the central anti-inflammatory response.
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