Cholecalciferol (vitamin D) has a direct protective activity against interleukin 6-induced atrophy in C2C12 myotubes.

We previously determined that different vitamin D metabolites can have opposite effects on C2C12 myotubes, depending on the sites of hydroxylation or doses. Specifically, 25(OH)D (25VD) has an anti-atrophic activity, 1,25(OH)D induces atrophy, and 24,25(OH)D is anti-atrophic at low concentrations and atrophic at high concentrations. This study aimed to clarify whether cholecalciferol (VD3) too, the non-hydroxylated upstream metabolite, has a direct effect on muscle cells.

Both ghrelin deletion and unacylated ghrelin overexpression preserve muscles in aging mice.

Sarcopenia, the decline in muscle mass and functionality during aging, might arise from age-associated endocrine dysfunction. Ghrelin is a hormone circulating in both acylated (AG) and unacylated (UnAG) forms with anti-atrophic activity on skeletal muscle. Here, we show that not only lifelong overexpression of UnAG (Tg) in mice, but also the deletion of ghrelin gene ( KO) attenuated the age-associated muscle atrophy and functionality decline, as well as systemic inflammation.

Haptoglobin Phenotypes Are Associated with the Postload Glucose and Insulin Levels in Pediatric Obesity.

Purpose: Haptoglobin (Hp) is a protein involved in the acute-phase reaction of inflammation. Humans have three major phenotypes (Hp1-1, Hp1-2, and Hp2-2). Several studies have shown altered Hp regulation in adults with obesity and metabolic alterations.

Identification of Haptoglobin as a Readout of rhGH Therapy in GH Deficiency.

Background: GH deficiency (GHD) is characterized by a cluster of cardiovascular risk factors and subtle inflammation. We aimed to demonstrate, through a proteomic approach, molecules directly modulated by GHD and involved in the inflammatory state.

Methods: Ten children with isolated GHD were studied before and after 1 year of treatment with rhGH and compared with 14 matched controls.

Opposing effects of 25-hydroxy- and 1α,25-dihydroxy-vitamin D on pro-cachectic cytokine-and cancer conditioned medium-induced atrophy in C2C12 myotubes.

Aim: Loss of skeletal muscle is one of the main features of cancer cachexia. Vitamin D (VD) deficiency is associated with impairment of muscle mass and performance and is highly prevalent in cachectic patients; therefore, VD supplementation has been proposed to counteract cancer cachexia-associated muscle loss. However, in both cachectic cancer patients and tumour-bearing animals, VD supplementation led to disappointing results, urging the need for a better understanding of VD activity on skeletal muscle.

Ghrelin knockout mice display defective skeletal muscle regeneration and impaired satellite cell self-renewal.

Purpose: Muscle regeneration depends on satellite cells (SCs), quiescent precursors that, in consequence of injury or pathological states such as muscular dystrophies, activate, proliferate, and differentiate to repair the damaged tissue. A subset of SCs undergoes self-renewal, thus preserving the SC pool and its regenerative potential. The peptides produced by the ghrelin gene, i.