A5070898685- Adipose Tissue and Metabolism
- Advanced Glycation End Products research
- Exercise and Physiological Responses
- Muscle Physiology and Disorders
- Diabetes, Cardiovascular Risks, and Lipoproteins
- Biochemical effects in animals
- Cardiovascular and exercise physiology
- Muscle metabolism and nutrition
- Sirtuins and Resveratrol in Medicine
- Mitochondrial Function and Pathology
- Diet and metabolism studies
- Nutrition and Health in Aging
- Diabetes Management and Research
- Dietary Effects on Health
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Neurogenetic and Muscular Disorders Research
- Healthcare and Venom Research
- Cardiovascular Health and Disease Prevention
- Ergonomics and Musculoskeletal Disorders
- Nitric Oxide and Endothelin Effects
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cardiac Health and Mental Health
- Redox biology and oxidative stress
- Alzheimer's disease research and treatments
- Ethics and bioethics in healthcare
University of Utah
2022-2025
University of Michigan
2018-2024
Michigan United
2023
Ann Arbor Center for Independent Living
2020
Washtenaw Community College
2019
University of Illinois Chicago
2016-2018
Salisbury University
2013-2017
Indo-American Center
2016
Reactive oxygen species (ROS) accumulation is a cardinal feature of skeletal muscle atrophy. ROS refers to collection radical molecules whose cellular signals are vast, and it unclear which downstream consequences responsible for the loss mass strength. Here, we show that lipid hydroperoxides (LOOH) increased with age disuse, LOOH by deletion glutathione peroxidase 4 (GPx4) sufficient augment promoted atrophy in lysosomal-dependent, proteasomal-independent manner. In young old mice, genetic...
The soluble receptor for advanced glycation end products (sRAGE) may be protective against inflammation associated with obesity and type 2 diabetes (T2DM). aim of this study was to determine the distribution sRAGE isoforms whether are risk T2DM development in subjects spanning glucose tolerance continuum. In retrospective analysis, circulating total endogenous secretory RAGE (esRAGE) were quantified via ELISA, cleaved (cRAGE) calculated 274 individuals stratified by status (GTS) obesity....
Insulin resistance promotes vascular endothelial dysfunction and subsequent development of cardiovascular disease. Previously we found that skeletal muscle arteriolar flow-induced dilation (FID) was reduced following a hyperinsulinemic clamp in healthy adults. Therefore, hypothesized hyperinsulinemia, hallmark insulin resistance, contributes to microvascular cell via inducing oxidative stress is mediated by NADPH oxidase (Nox) system. We examined the effect insulin, at levels are comparable...
Cathepsin B (CTSB) and brain derived neurotrophic factor (BDNF) are increased with aerobic exercise (AE) skeletal muscle has been identified as a potential source of secretion. However, the intensity AE for contributions to circulating CTSB BDNF have not fully studied in humans.Determine effects on expression profiles.Young healthy subjects (n = 16) completed treadmill-based consisting VO2max calorie-matched acute sessions at 40%, 65% 80% VO2max. Fasting serum was obtained before 30-minutes...
Immobilization-associated muscle atrophy and weakness appear to be driven in part by oxidative stress. Nuclear Factor Erythroid 2-Related 2 (NRF2) is a critical redox rheostat that regulates stress responses, its deletion known accelerate during aging (sarcopenia) or denervation. Conversely, pharmacologic activation of NRF2 extends mouse lifespan attenuates sarcopenia. Similarly, Kelch-like ECH-associated Protein 1 (Keap1), negative regulator NRF2, enhances exercise capacity. The purpose...
Skeletal muscle insulin resistance is a hallmark of Type 2 diabetes (T2DM) and may be exacerbated by protein modifications methylglyoxal (MG), known as dicarbonyl stress. The glyoxalase enzyme system composed 1/2 (GLO1/GLO2) the natural defense against stress, yet its expression, activity, regulation remain largely unexplored in skeletal muscle. Therefore, this study investigated stress subjects with T2DM (age: 56 ± 5 yr.; BMI: 32 kg/m ) compared lean healthy control (LHC; age: 27 1 22 )....
The purpose of this investigation was to evaluate the effects experimental hyperglycemia on oxidative damage (OX), advanced glycation end products (AGEs), and receptor for AGEs (RAGE) through an in vivo approach. Obese subjects (n = 10; 31.2 ± 1.2 kg·m−2; 56 3 years) underwent 24 h hyperglycemic clamp (+5.4 mM above basal), where plasma at basal after 2 challenge were assayed OX (methionine sulfoxide, MetSO, aminoadipic acid, AAA) AGE-free adducts (Ne-carboxymethyllysine, CML;...
Although there is evidence for metabolic dysfunction and chronic inflammation in Alzheimer’s disease (AD), circulating levels of soluble receptor advanced glycation end products (sRAGE) the (RAGE) ligand S100B have not been characterized. sRAGE an important mediator as it can act a decoy RAGE attenuate downstream inflammatory signaling. Cognitively healthy elderly AD participants with without type 2 diabetes (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"...
Advanced glycation end products (AGEs) promote the development of diabetic complications through activation their receptor (RAGE). Isoforms soluble RAGE (sRAGE) sequester AGEs and protect against RAGE-mediated complications. We investigated effect an overnight fast on circulating metabolic substrates, hormones, AGEs, sRAGE isoforms in 26 individuals with type 1 diabetes (T1DM). Blood was collected from young (18⁻30 years) T1DM patients insulin pumps before after fast. Circulating were...
This study is the first to investigate effects of aerobic exercise intensity on circulating sRAGE isoforms, muscle RAGE protein, and splicing. isoforms tended diminish with exercise, although this effect was attenuated increasing intensity. Muscle protein gene expression were unaffected by exercise. However, individuals obesity displayed nearly twofold higher expression, which positively correlated P65 subunit NF-κB.
The benefits of exercise involve skeletal muscle redox state alterations nicotinamide adenine dinucleotide (NAD) and flavin (FAD). We determined the fiber-specific effects acute on in healthy adults. Muscle biopsies were obtained from 19 participants (11 M, 8 F; 26 ± 4 yr) at baseline (fasted) 30 min 3 h after treadmill 80% maximal oxygen consumption (V̇o
A high-fat diet can induce inflammation and metabolic diseases such as diabetes atherosclerosis. The receptor for advanced glycation endproducts (RAGE) plays a critical role in disease pathophysiology the soluble form of (sRAGE) mitigate these effects. However, little is known about RAGE postprandial condition effect exercise this context. Thus, we aimed to determine effects single meal (HFM) with without prior on peripheral blood mononuclear cell (PBMC) biology. Healthy males (n = 12)...
Thioredoxin-interacting protein (TXNIP) negatively effects the redox state and growth signaling via its interactions with thioredoxin (TRX) regulated in development DNA damage response 1 (REDD1), respectively. TXNIP expression is downregulated by pathways activated during aerobic exercise (AE), posttranslational modifications (PTMs; serine phosphorylation ubiquitination). The purpose of this investigation was to determine acute AE on expression, modifications, interacting partners, REDD1...
The receptor for advanced glycation end products (RAGE) is a transmembrane that upon binding of its ligand induces inflammation and promotes the development complications associated with obesity, diabetes, aging. Soluble isoforms RAGE (sRAGE) produced by proteolytic cleavage (sRAGEc) or alternative splicing (endogenous secretory RAGE, esRAGE), inhibit signaling scavenging ligands. plays role in adipocyte hypertrophy individuals obesity present lower circulating levels sRAGE. This phenotype...
The goal of this investigation was to evaluate circulating and skeletal muscle inflammatory biomarkers between maintenance hemodialysis (MHD) demographic-matched control subjects (CON) before after ingestion a protein-rich meal.CON (n = 8; 50 ± 2 years; 31 1 kg/m2) MHD patients 56 5 32 underwent basal blood draw biopsy serial draws the mixed meal on nondialysis day. Plasma advanced glycation end products (AGEs) markers oxidation were assessed via liquid chromatography-tandem mass...
With a globally aging population, the need for treatments that address age related comorbidities are more relevant than ever. Previous research done in our lab has shown treatment of mice with compound N-Acetyl-Carnosine (N-Ac-Carn) could partially prevent protein damage caused by lipid peroxidation, and subsequent muscle atrophy weakness mouse-model inactivity. N-Ac-Carn is endogenously produced, safe, affordable making it potentially promising strategy age-related functional decline. Our...
By 2050 the number of individuals over age 80y will triple to reach 426 million and rate age-related comorbidities has also increased precipitously as our global population continued age. Currently, there is no clinically approved treatment for functional decline creating demand development such treatments. Our lab previously demonstrated that carbonyl stress exacerbated in muscles during a hindlimb unloading (HU) model inactivity. Importantly, accumulation proteins modified by reactive...
Glyoxalase I (GLO1) is the primary enzyme for detoxification of reactive dicarbonyl methylglyoxal (MG). Loss GLO1 promotes accumulation MG resulting in a recapitulation diabetic phenotypes. We previously demonstrated attenuated protein skeletal muscle from individuals with type 2 diabetes (T2D). However, whether attenuation occurs prior to T2D and mechanisms regulating abundance are unknown. expression activity were determined tissue biopsies 15 lean healthy (LH, BMI: 22.4 ± 0.7) 5 obesity...
Abstract Immobilization-associated muscle atrophy and weakness appear to be driven in part by oxidative stress. Nuclear Factor Erythroid 2-Related 2 (NRF2) is a critical redox rheostat that regulates stress responses, its deletion known accelerate during aging (sarcopenia) or denervation. Conversely, pharmacologic activation of NRF2 extends mouse lifespan attenuates sarcopenia. Similarly, Kelch-like ECH-associated Protein 1 (Keap1), negative regulator NRF2, enhances exercise capacity. The...
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a progressive disorder marked by lipid accumulation, leading to steatohepatitis (MASH). A key feature of the transition MASH involves oxidative stress resulting from defects in mitochondrial phosphorylation (OXPHOS). Here, we show that pathological alterations composition inner membrane (IMM) directly instigate electron transfer inefficiency promote stress. Specifically, cardiolipin (CL) was downregulated with MASLD/MASH...