- Physical inactivity and knee osteoarthritis in guinea pigs. [Journal Article]
- OCOsteoarthritis Cartilage 2019 Jul 11
- CONCLUSIONS: Our findings indicate that a sedentary lifestyle promotes the development of knee OA, particularly by enhancing disease severity rather than risk of onset, and this potentially occurs through multiple pathways including by engendering growth of functionally deficient joint tissues and the accumulation of excess body weight and adiposity.
- Electric pulse stimulation inhibited lipid accumulation on C2C12 myotubes incubated with oleic acid and palmitic acid. [Journal Article]
- APArch Physiol Biochem 2019 Jul 12; :1-7
- CONCLUSIONS: EPS reduced lipid droplet accumulation; enhanced CD36, FATP4, FABP1 and FABP5 expression; inhibited C2C12 myotube fatty acid re-esterification; and promoted fatty acid oxidation in C2C12 myotubes.
- Long-term voluntary wheel running does not alter vascular amyloid burden but reduces neuroinflammation in the Tg-SwDI mouse model of cerebral amyloid angiopathy. [Journal Article]
- JNJ Neuroinflammation 2019 Jul 11; 16(1):144
- CONCLUSIONS: Taken together, these results suggest that CAA can still develop regardless of a lifespan of substantial CVE, although downstream effects on neuroinflammation may be reduced and functional outcomes improved.
- Chronic exercise training prevents coronary artery stiffening in aortic-banded miniswine: Role of perivascular adipose-derived advanced glycation end products. [Journal Article]
- JAJ Appl Physiol (1985) 2019 Jul 11
- Aims Heart failure (HF) is associated with increased large conduit artery stiffness and afterload resulting in stiffening of the coronary arteries. Perivascular adipose tissue (PVAT) and advanced gly…
Aims Heart failure (HF) is associated with increased large conduit artery stiffness and afterload resulting in stiffening of the coronary arteries. Perivascular adipose tissue (PVAT) and advanced glycation end products (AGE) both promote arterial stiffness, yet the mechanisms by which coronary PVAT promotes arterial stiffness and the efficacy of exercise to prevent coronary stiffness are unknown. We hypothesized both chronic continuous and interval exercise training would prevent coronary PVAT-mediated AGE secretion and arterial stiffness. Methods and Results Yucatan mininature swine were divided into four groups: control-sedentary (CON), aortic-banded sedentary heart failure (HF), aortic-banded HF continuous exercise trained (HF+CONT), and aortic-banded HF interval exercise trained (HF+IT). The left circumflex (LCX) and right coronary artery (RCA) underwent ex vivo mechanical testing, and arterial AGE, elastin and collagen were assessed. Coronary elastin elastic modulus (EEM) and elastin protein were lower, and AGE was increased with HF compared to CON that was prevented by both HF+CONT and HF+IT. Mouse aortic segments treated with swine coronary PVAT-conditioned media had lower EEM, elastin content, greater AGE secretion and arterial AGE accumulation in HF compared with CON, which was prevented by both HF+CONT and HF+IT. Aminoguanidine (AMG), an AGE inhibitor, prevented the reduction in the EEM, arterial elastin content and AGE accumulation in mouse aortic segments treated with PVAT conditioned media in the HF group. Conclusions Our data demonstrate efficacy for chronic continuous and interval exercise to prevent coronary artery stiffness via inhibition of PVAT-derived AGE secretion in a pre-clinical mini-swine model of pressure overload-induced HF.
- The mitochondrial-derived peptide MOTS-c is a regulator of plasma metabolites and enhances insulin sensitivity. [Journal Article]
- PRPhysiol Rep 2019; 7(13):e14171
- MOTS-c is an exercise mimetic and improves insulin sensitivity in aged and diet-induced obese mice. Although plasma markers are good markers for the metabolic condition, whether MOTS-c changes plasma…
MOTS-c is an exercise mimetic and improves insulin sensitivity in aged and diet-induced obese mice. Although plasma markers are good markers for the metabolic condition, whether MOTS-c changes plasma markers in diet-induced obese mice has not been examined. Here, we used an unbiased metabolomics approach to examine the effect of MOTS-c on plasma markers of metabolic dysfunction. We found that three pathways - sphingolipid metabolism, monoacylglycerol metabolism, and dicarboxylate metabolism - were reduced in MOTS-c-injected mice. Interestingly, these pathways are upregulated in obese and T2D models. MOTS-c improves insulin sensitivity and increases beta-oxidation to prevent fat accumulation in DIO mice through these pathways. These results provide us a better understanding of the mechanism of how MOTS-c improves insulin sensitivity and reduces the body weight and fatty liver and opens a new venue for further study.
- Phosphatidylserine decarboxylase is critical for the maintenance of skeletal muscle mitochondrial integrity and muscle mass. [Journal Article]
- MMMol Metab 2019 Jun 27
- CONCLUSIONS: The PSD pathway has a significant role in maintaining phospholipid homeostasis in adult skeletal muscle. Moreover, PSD is essential for maintenance of mitochondrial integrity and skeletal muscle mass.
- Clinical impact of sarcopenia and dynapenia on diabetes. [Editorial]
- DIDiabetol Int 2019; 10(3):183-187
- Sarcopenia as a progressive and generalized skeletal muscle disorder that is associated with an increased likelihood of adverse outcomes, including falls, fractures, physical disability, and mortalit…
Sarcopenia as a progressive and generalized skeletal muscle disorder that is associated with an increased likelihood of adverse outcomes, including falls, fractures, physical disability, and mortality. On the other hand, an age-related decline in muscle strength prior to the reduction of muscle mass, is proposed to be "dynapenia". Sarcopenia and dynapenia have recently been recognized as a diabetic complications in type 2 diabetes. We firstly indicated that sarcopenia was frequently observed in 16.6% of patients with type 1 diabetes aged even over 40 years. Additionally, we recently reported that the prevalence rate of dynapenia was higher than sarcopenia in patients with type 2 diabetes. Chronic hyperglycemia accelerates accumulation of advanced glycation end products (AGEs), which causes diabetic vascular complications through oxidative stress and chronic inflammation. We also demonstrated that skin autofluorescence (AF) as a marker of AGEs, was the independent determinant for skeletal muscle mass and strength in patients with type 2 diabetes and muscle strength in type 1 diabetes. Therefore, the early diagnosis of muscle weakness is essential for patients with diabetes and sustained good glycemic control with exercise and dietary intervention might be beneficial to prevent the progression of muscle weakness in these patients.
- Physical activity and sedentary activity: population epidemiology and concordance in Australian children aged 11-12 years and their parents. [Journal Article]
- BOBMJ Open 2019 Jul 04; 9(Suppl 3):136-146
- CONCLUSIONS: Standardised cutpoints are needed for objective activity measures to inform activity guidelines across the lifecourse. This may reflect large amounts of time in non-shared environments (school and work).
- Effect of Aerobic and Resistance Exercise on Cardiac Adipose Tissues: Secondary Analyses From a Randomized Clinical Trial. [Journal Article]
- JCJAMA Cardiol 2019 Jul 03
- CONCLUSIONS: In individuals with abdominal obesity, both endurance and resistance training reduced epicardial adipose tissue mass, while only resistance training reduced pericardial adipose tissue mass. These data highlight the potential preventive importance of different exercise modalities as means to reduce cardiac fat in individuals with abdominal obesity.
New Search Next
- Obesity Alters the Muscle Protein Synthetic Response to Nutrition and Exercise. [Review]
- FNFront Nutr 2019; 6:87
- Improving the health of skeletal muscle is an important component of obesity treatment. Apart from allowing for physical activity, skeletal muscle tissue is fundamental for the regulation of postpran…
Improving the health of skeletal muscle is an important component of obesity treatment. Apart from allowing for physical activity, skeletal muscle tissue is fundamental for the regulation of postprandial macronutrient metabolism, a time period that represents when metabolic derangements are most often observed in adults with obesity. In order for skeletal muscle to retain its capacity for physical activity and macronutrient metabolism, its protein quantity and composition must be maintained through the efficient degradation and resynthesis for proper tissue homeostasis. Life-style behaviors such as increasing physical activity and higher protein diets are front-line treatment strategies to enhance muscle protein remodeling by primarily stimulating protein synthesis rates. However, the muscle of individuals with obesity appears to be resistant to the anabolic action of targeted exercise regimes and protein ingestion when compared to normal-weight adults. This indicates impaired muscle protein remodeling in response to the main anabolic stimuli to human skeletal muscle tissue is contributing to poor muscle health with obesity. Deranged anabolic signaling related to insulin resistance, lipid accumulation, and/or systemic/muscle inflammation are likely at the root of the anabolic resistance of muscle protein synthesis rates with obesity. The purpose of this review is to discuss the impact of protein ingestion and exercise on muscle protein remodeling in people with obesity, and the potential mechanisms underlining anabolic resistance of their muscle.