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Kevin C. Baker - One of the best experts on this subject based on the ideXlab platform.
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Traumatic Joint Injury Induces Acute Catabolic Bone Turnover Concurrent with Articular Cartilage Damage in a Rat Model of Post-Traumatic Osteoarthritis.
Journal of Orthopaedic Research, 2020Co-Authors: Tristan Maerz, Michael D. Newton, Mackenzie M. Fleischer, Samantha E. Hartner, Karissa Gawronski, Lucas Junginger, Kevin C. BakerAbstract:Assess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR). Twelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n=6/group). In vivo μCT was performed at 3, 7, 10, and 14 days post-injury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone Anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and articular cartilage morphology was quantified using ex vivo μCT and contrast-enhanced µCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections. ACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days post-injury, while lateral femoral condyles (LFC) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone Anabolism (~15-20%), and a ~32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, cartilage thickness, and cartilage surface deviation. ACL rupture induces immediate and sustained reduction of bone Anabolism and overactivation of bone catabolism, with mild-to-moderate articular cartilage damage at 14 days post-injury. This article is protected by copyright. All rights reserved.
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traumatic joint injury induces acute catabolic bone turnover concurrent with articular cartilage damage in a rat model of post traumatic osteoarthritis
Journal of Orthopaedic Research, 2020Co-Authors: Tristan Maerz, Michael D. Newton, Mackenzie M. Fleischer, Samantha E. Hartner, Karissa Gawronski, Lucas Junginger, Kevin C. BakerAbstract:Assess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR). Twelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n = 6/group). In vivo μCT was performed at 3, 7, 10, and 14 days postinjury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone Anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and articular cartilage morphology was quantified using ex vivo μCT and contrast-enhanced µCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections. ACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days postinjury, while lateral femoral condyles (LFCs) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone Anabolism (~15%-20%), and a ~32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, cartilage thickness, and cartilage surface deviation. ACL rupture induces immediate and sustained reduction of bone Anabolism and overactivation of bone catabolism, with mild-to-moderate articular cartilage damage at 14 days postinjury.
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Traumatic Joint Injury Induces Acute Catabolic Bone Turnover Concurrent with Articular Cartilage Damage in a Rat Model of Post-Traumatic Osteoarthritis
2020Co-Authors: Tristan Maerz, Michael D. Newton, Mackenzie M. Fleischer, Samantha E. Hartner, Karissa Gawronski, Lucas Junginger, Kevin C. BakerAbstract:Objective: Assess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR). Methods: Twelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n=6/group). In vivo microCT was performed at 3, 7, 10, and 14 days post-injury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone Anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and articular cartilage morphology was quantified using ex vivo microCT and contrast-enhanced microCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections. Results: ACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days post-injury, while lateral femoral condyles (LFC) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone Anabolism (~15-20%), and a ~32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, cartilage thickness, and cartilage surface deviation. Conclusion: ACL rupture induces immediate and sustained reduction of bone Anabolism and overactivation of bone catabolism, with mild-to-moderate articular cartilage damage at 14 days post-injury.
Réjeanne Gougeon - One of the best experts on this subject based on the ideXlab platform.
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Muscle protein Anabolism in type 2 diabetes
Current opinion in clinical nutrition and metabolic care, 2013Co-Authors: Maya Bassil, Réjeanne GougeonAbstract:Purpose of review Protein Anabolism is abnormal in human type 2 diabetes (T2DM). We review studies of anabolic stimuli that identify potential causes. If uncorrected, and combined with aging effects, they will compromise muscle function and mass. Knowing causes can guide studies of preventive and treatment measures. Recent findings T2DM accelerates age-related decreases in muscle mass. This could be related to insulin resistance of whole-body protein Anabolism demonstrated in hyperglycemic obese men. In contrast, their protein anabolic response to hyperaminoacidemia suggested that ample amino acid administration, especially branched chain amino acids might overcome such insulin resistance. One study of chronic leucine supplementation in elderly T2DM patients did not increase muscle mass. However, they lacked sarcopenia and had adequate dietary protein intake, so may be atypical. Exercise induced similar increases in muscle protein synthesis, mass and strength in healthy and T2DM patients suggesting that physical activity might also overcome insulin resistance of protein Anabolism. Summary Muscle protein Anabolism in T2DM is resistant to the action of insulin but perhaps not to amino acid supply or exercise. Whether leucine supplementation improves muscle mass and function in persons with T2DM (especially elderly) with reduced protein intake or muscle mass needs to be determined.
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Postprandial hyperaminoacidaemia overcomes insulin resistance of protein Anabolism in men with type 2 diabetes
Diabetologia, 2010Co-Authors: Maya Bassil, Stéphanie Chevalier, José A. Morais, Errol B. Marliss, S Pereira, Réjeanne GougeonAbstract:Aims/hypothesis Although protein is usually ignored when considering insulin resistance, we have shown resistance of protein concurrent with glucose metabolism in men with type 2 diabetes during a hyperinsulinaemic clamp at euglycaemia and fasting aminoacidaemia. We hypothesised that this resistance is even worse during conditions that simulate the postprandial state, when Anabolism should be maximal.
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Fed-state clamp stimulates cellular mechanisms of muscle protein Anabolism and modulates glucose disposal in normal men
American journal of physiology. Endocrinology and metabolism, 2008Co-Authors: Olasunkanmi A. J. Adegoke, Stéphanie Chevalier, Réjeanne Gougeon, José A. Morais, Scot R. Kimball, Leonard S. Jefferson, Simon S. Wing, Errol B. MarlissAbstract:Since maximum Anabolism occurs postprandially, we developed a simulated fed state with clamped hyperinsulinemia, physiological hyperglycemia, and hyperaminoacidemia (Hyper-3) and explored muscle ce...
Maya Bassil - One of the best experts on this subject based on the ideXlab platform.
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Muscle protein Anabolism in type 2 diabetes
Current opinion in clinical nutrition and metabolic care, 2013Co-Authors: Maya Bassil, Réjeanne GougeonAbstract:Purpose of review Protein Anabolism is abnormal in human type 2 diabetes (T2DM). We review studies of anabolic stimuli that identify potential causes. If uncorrected, and combined with aging effects, they will compromise muscle function and mass. Knowing causes can guide studies of preventive and treatment measures. Recent findings T2DM accelerates age-related decreases in muscle mass. This could be related to insulin resistance of whole-body protein Anabolism demonstrated in hyperglycemic obese men. In contrast, their protein anabolic response to hyperaminoacidemia suggested that ample amino acid administration, especially branched chain amino acids might overcome such insulin resistance. One study of chronic leucine supplementation in elderly T2DM patients did not increase muscle mass. However, they lacked sarcopenia and had adequate dietary protein intake, so may be atypical. Exercise induced similar increases in muscle protein synthesis, mass and strength in healthy and T2DM patients suggesting that physical activity might also overcome insulin resistance of protein Anabolism. Summary Muscle protein Anabolism in T2DM is resistant to the action of insulin but perhaps not to amino acid supply or exercise. Whether leucine supplementation improves muscle mass and function in persons with T2DM (especially elderly) with reduced protein intake or muscle mass needs to be determined.
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Postprandial hyperaminoacidaemia overcomes insulin resistance of protein Anabolism in men with type 2 diabetes
Diabetologia, 2010Co-Authors: Maya Bassil, Stéphanie Chevalier, José A. Morais, Errol B. Marliss, S Pereira, Réjeanne GougeonAbstract:Aims/hypothesis Although protein is usually ignored when considering insulin resistance, we have shown resistance of protein concurrent with glucose metabolism in men with type 2 diabetes during a hyperinsulinaemic clamp at euglycaemia and fasting aminoacidaemia. We hypothesised that this resistance is even worse during conditions that simulate the postprandial state, when Anabolism should be maximal.
Elena Volpi - One of the best experts on this subject based on the ideXlab platform.
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skeletal muscle amino acid transporter expression is increased in young and older adults following resistance exercise
Journal of Applied Physiology, 2011Co-Authors: Micah J Drummond, Elena Volpi, Erin L Glynn, Kyle L Timmerman, Christopher S Fry, Jared M Dickinson, Dillon K Walker, David M Gundermann, Blake B RasmussenAbstract:Amino acid transporters and mammalian target of rapamycin complex 1 (mTORC1) signaling are important contributors to muscle protein Anabolism. Aging is associated with reduced mTORC1 signaling foll...
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supraphysiological hyperinsulinaemia is necessary to stimulate skeletal muscle protein Anabolism in older adults evidence of a true age related insulin resistance of muscle protein metabolism
Diabetologia, 2009Co-Authors: Satoshi Fujita, Erin L Glynn, Kyle L Timmerman, Blake B Rasmussen, Elena VolpiAbstract:Aims/hypothesis The physiological increase in muscle protein Anabolism induced by insulin is blunted in healthy, glucose-tolerant older adults. We hypothesised that the age-related defect in muscle protein Anabolism is a true insulin resistance state and can be overridden by supraphysiological hyperinsulinaemia.
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effect of insulin on human skeletal muscle protein synthesis is modulated by insulin induced changes in muscle blood flow and amino acid availability
American Journal of Physiology-endocrinology and Metabolism, 2006Co-Authors: Blake B Rasmussen, Satoshi Fujita, Jerson G Cadenas, James J Grady, Elena VolpiAbstract:Insulin promotes muscle Anabolism, but it is still unclear whether it stimulates muscle protein synthesis in humans. We hypothesized that insulin can increase muscle protein synthesis only if it in...
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essential amino acids are primarily responsible for the amino acid stimulation of muscle protein Anabolism in healthy elderly adults
The American Journal of Clinical Nutrition, 2003Co-Authors: Elena Volpi, Robert R Wolfe, Hisamine Kobayashi, Melinda Sheffieldmoore, Bettina MittendorferAbstract:Background: Nutritional supplementation may be used to treat muscle loss with aging (sarcopenia). However, if physical activity does not increase, the elderly tend to compensate for the increased energy delivered by the supplements with reduced food intake, which results in a calorie substitution rather than supplementation. Thus, an effective supplement should stimulate muscle Anabolism more efficiently than food or common protein supplements. We have shown that balanced amino acids stimulate muscle protein Anabolism in the elderly, but it is unknown whether all amino acids are necessary to achieve this effect. Objective: We assessed whether nonessential amino acids are required in a nutritional supplement to stimulate muscle protein Anabolism in the elderly. Design: We compared the response of muscle protein metabolism to either 18 g essential amino acids (EAA group: n = 6, age 69 ± 2 y; x ± SD) or 40 g balanced amino acids (18 g essential amino acids + 22 g nonessential amino acids, BAA group; n = 8, age 71 ± 2 y) given orally in small boluses every 10 min for 3 h to healthy elderly volunteers. Muscle protein metabolism was measured in the basal state and during amino acid administration via L-[ring- 2 H5]phenylalanine infusion, femoral arterial and venous catheterization, and muscle biopsies. Results: Phenylalanine net balance (in nmol · min � 1 · 100 mL leg volume � 1 ) increased from the basal state (P < 0.01), with no differences between groups (BAA: from � 16 ± 5 to 16 ± 4; EAA: from � 18 ± 5 to 14 ± 13) because of an increase (P < 0.01) in muscle protein synthesis and no change in breakdown. Conclusion: Essential amino acids are primarily responsible for the amino acid‐induced stimulation of muscle protein Anabolism in the elderly. Am J Clin Nutr 2003;78:250‐8.
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Androstenedione does not stimulate muscle protein Anabolism in young healthy men
The Journal of clinical endocrinology and metabolism, 2000Co-Authors: Blake B Rasmussen, Elena Volpi, Dennis C. Gore, Robert R WolfeAbstract:Androstenedione is the immediate precursor of testosterone. Androstenedione intake has been speculated to increase plasma testosterone levels and muscle Anabolism. Thus, androstenedione supplements have become widely popular in the sport community to improve performance. This study was designed to determine whether 5 days of oral androstenedione (100 mg/day) supplementation increases skeletal muscle Anabolism. Six healthy young men were studied before the treatment period and after 5 days of oral androstenedione supplementation. Muscle protein turnover parameters were compared to those of a control group studied twice as well and receiving no treatment. We measured muscle protein kinetics using a three-compartment model involving infusion of l-[ring-2H5]phenylalanine, blood sampling from femoral artery and vein, and muscle biopsies. Plasma testosterone, androstenedione, LH, and estradiol concentrations were determined by RIA. After ingestion of oral androstenedione, plasma testosterone and LH concentratio...
Tristan Maerz - One of the best experts on this subject based on the ideXlab platform.
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Traumatic Joint Injury Induces Acute Catabolic Bone Turnover Concurrent with Articular Cartilage Damage in a Rat Model of Post-Traumatic Osteoarthritis.
Journal of Orthopaedic Research, 2020Co-Authors: Tristan Maerz, Michael D. Newton, Mackenzie M. Fleischer, Samantha E. Hartner, Karissa Gawronski, Lucas Junginger, Kevin C. BakerAbstract:Assess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR). Twelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n=6/group). In vivo μCT was performed at 3, 7, 10, and 14 days post-injury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone Anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and articular cartilage morphology was quantified using ex vivo μCT and contrast-enhanced µCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections. ACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days post-injury, while lateral femoral condyles (LFC) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone Anabolism (~15-20%), and a ~32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, cartilage thickness, and cartilage surface deviation. ACL rupture induces immediate and sustained reduction of bone Anabolism and overactivation of bone catabolism, with mild-to-moderate articular cartilage damage at 14 days post-injury. This article is protected by copyright. All rights reserved.
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traumatic joint injury induces acute catabolic bone turnover concurrent with articular cartilage damage in a rat model of post traumatic osteoarthritis
Journal of Orthopaedic Research, 2020Co-Authors: Tristan Maerz, Michael D. Newton, Mackenzie M. Fleischer, Samantha E. Hartner, Karissa Gawronski, Lucas Junginger, Kevin C. BakerAbstract:Assess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR). Twelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n = 6/group). In vivo μCT was performed at 3, 7, 10, and 14 days postinjury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone Anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and articular cartilage morphology was quantified using ex vivo μCT and contrast-enhanced µCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections. ACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days postinjury, while lateral femoral condyles (LFCs) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone Anabolism (~15%-20%), and a ~32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, cartilage thickness, and cartilage surface deviation. ACL rupture induces immediate and sustained reduction of bone Anabolism and overactivation of bone catabolism, with mild-to-moderate articular cartilage damage at 14 days postinjury.
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Traumatic Joint Injury Induces Acute Catabolic Bone Turnover Concurrent with Articular Cartilage Damage in a Rat Model of Post-Traumatic Osteoarthritis
2020Co-Authors: Tristan Maerz, Michael D. Newton, Mackenzie M. Fleischer, Samantha E. Hartner, Karissa Gawronski, Lucas Junginger, Kevin C. BakerAbstract:Objective: Assess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR). Methods: Twelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n=6/group). In vivo microCT was performed at 3, 7, 10, and 14 days post-injury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone Anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and articular cartilage morphology was quantified using ex vivo microCT and contrast-enhanced microCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections. Results: ACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days post-injury, while lateral femoral condyles (LFC) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone Anabolism (~15-20%), and a ~32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, cartilage thickness, and cartilage surface deviation. Conclusion: ACL rupture induces immediate and sustained reduction of bone Anabolism and overactivation of bone catabolism, with mild-to-moderate articular cartilage damage at 14 days post-injury.