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Many diseases are associated with catabolic conditions that induce skeletal muscle wasting. These various catabolic states may have similar and distinct mechanisms for inducing muscle protein loss. Mechanisms related to muscle wasting may also be related to muscle metabolism since glycolytic muscle fibers have greater wasting susceptibility with several(More)
Although testosterone administration elicits well-documented anabolic effects on skeletal muscle mass, the enhancement of muscle regeneration after injury has not been widely examined. The purpose of this study was to determine whether anabolic steroid administration improves skeletal muscle regeneration from bupivacaine-induced injury. Male C57BL/6 mice(More)
BACKGROUND The loss of dystrophin compromises muscle cell membrane stability and causes Duchenne muscular dystrophy and/or various forms of cardiomyopathy. Increased expression of the dystrophin homolog utrophin by gene delivery or pharmacologic up-regulation has been demonstrated to restore membrane integrity and improve the phenotype in the(More)
BACKGROUND Cachexia involves unintentional body weight loss including diminished muscle and adipose tissue mass and is associated with an underlying disease. Systemic overexpression of IL-6 accelerates cachexia in the Apc(Min/+) mouse, but does not induce wasting in control C57BL/6 mice. With many chronic diseases, chronic inflammation and metabolic(More)
BACKGROUND Estrogens are associated with the loss of skeletal muscle strength in women with age. Ovarian hormone removal by ovariectomy in mice leads to a loss of muscle strength, which is reversed with 17beta-estradiol replacement. Aging is also associated with an increase in antioxidant stress, and estrogens can improve antioxidant status via their(More)
The Apc Min/+ mouse has a mutation in the Apc tumor suppressor gene and develops intestinal polyps, beginning at 4 weeks of age. This mouse develops cachexia by 6 months, characterized by significant loss of muscle and fat tissue. The purpose of the present study was to determine the role of circulating IL-6 and the polyp burden for the development of(More)
Aging can alter the skeletal muscle growth response induced by overload. The initiation of overload induces muscle extracellular matrix expansion, increased cellularity, and inflammatory gene expression, which are all related to processes important for myofiber growth. These remodeling processes are also biological targets of testosterone. It is not certain(More)
Many epidemiological studies have demonstrated that level of exercise is associated with reduced colorectal cancer risk. Treadmill training can decrease Apc(Min/+) mouse intestinal polyp number and size, but the mechanisms remain unclear. Understanding the molecular changes in the tumor following exercise training may provide insight on the mechanism by(More)
The primary purpose of this study was to determine if tibial bone strength is compromised in dystrophic mice and if so, what geometric and material properties contribute. Results of three-point bending tests showed that tibia of mdx and dko (dystrophin- and utrophin-deficient) mice had up to 50% lower strength and stiffness compared to wild-type mice.(More)
OBJECTIVES The purpose of this study was to determine the extent to which prednisolone treatment and restricted physical activity caused deleterious changes in inherently compromised mdx bone. METHODS Four week-old male mdx mice (n=36) were treated for 8-wk either with or without prednisolone (0.8-1.3 mg/kg/d) and were housed in traditional or small cages(More)