transforming-growth-factor-beta and Malnutrition

Alcoholic liver disease remains a frequent and serious problem for increasing numbers of patients. Research has expanded our molecular understanding of the cellular basis of disease progression; however, translation into therapy is still hampered by a lack of suitable animal models for alcoholic liver disease, as well as from consequences of related liver damage due to malnutrition, hepatitis C virus infection, or abuse of other substances. Many patients with liver disease do not simply consume too much alcohol; they also suffer from comorbidities such as obesity or viral hepatitis, and/or may be addicted to other drugs besides alcohol. This review will summarize the currently available animal models to study liver disease due to either single causes or combinations of liver toxic substances/infections and alcohol.

Topics: Animals; Cytochrome P-450 CYP2E1; Disease Models, Animal; Hepatitis C, Chronic; Humans; Liver; Liver Diseases, Alcoholic; Malnutrition; Obesity, Morbid; Transforming Growth Factor beta

Protein-energy malnutrition and specific nutrient deficiencies are common in inflammatory bowel diseases (IBD), more particularly in Crohn's disease. In adults, the use of artificial nutrition is indicated in the event of malnutrition, short bowel syndrome, or IBD refractory to all other treatments. In children, enteral nutrition has a place as first-line treatment to avoid side effects of corticosteroids on growth. The use, as a therapeutic tool, of specific nutrients (n-3 fatty acids, glutamine, antioxydant vitamins and minerals, TGF-beta, probiotics...) seems interesting at the pathophysiological level. Nevertheless, these nutrients are still under evaluation and there are not enough available studies to recommend them in clinical routine. A very promising solution is the use of probiotics for the treatment of refractory pouchitis.

Topics: Antioxidants; Enteral Nutrition; Fatty Acids, Omega-3; Glutamine; Humans; Inflammatory Bowel Diseases; Malnutrition; Probiotics; Secondary Prevention; Transforming Growth Factor beta

Topics: Adolescent; Child; Colitis, Ulcerative; Crohn Disease; Enteral Nutrition; Female; Growth Disorders; Hematologic Tests; Humans; Male; Malnutrition; Remission Induction; Retrospective Studies; Transforming Growth Factor beta

Loss of skeletal muscle mass is a poorly understood complication of end-stage liver disease (ESLD). Based on recent stem cell literature, we hypothesized that the potent negative regulator of muscle mass, myostatin, could play a role in the muscle loss associated with ESLD. In this preliminary investigation, we measured myostatin levels in patients undergoing liver transplant evaluation, using a novel enzyme-linked immunosensitivity assay. Myostatin levels were significantly elevated in patients with ESLD compared with healthy controls. These data suggest that myostatin deserves further investigation as a target for therapies designed to preserve muscle mass in patients with ESLD.

Topics: Enzyme-Linked Immunosorbent Assay; Female; Humans; Liver Failure; Liver Transplantation; Male; Malnutrition; Middle Aged; Muscular Diseases; Myostatin; Prothrombin Time; Reverse Transcriptase Polymerase Chain Reaction; Transforming Growth Factor beta; Wasting Syndrome

To determine the roles of myostatin and insulin-like growth factor-I (IGF-I) during postnatal growth, we examined IGF-I and myostatin mRNA expression in the skeletal muscles of hypophysectomized and underfed rats during postnatal growth.. Five-week-old rats were divided into four groups: freely fed control, moderately underfed, severely underfed and hypophysectomized. Four weeks later, blood and muscle samples were gathered to determine serum IGF-I, myosin heavy chain (MHC) isoforms, IGF-I Ea, IGF-I Eb and myostatin mRNA.. The weights of soleus, plantaris and masseter muscles were decreased in underfed and hypophysectomized rats. Hypophysectomy resulted in significant increases of type I MHC at the expense of type IIx in plantaris muscle and of neonatal MHC at the expense of types IIx and IIb in masseter muscle. Serum IGF-I was decreased by underfeeding and hypophysectomy. Plantaris muscle IGF-I Ea mRNA in underfed and hypophysectomized rats was significantly lower than in normal controls. Plantaris muscle IGF-I Eb mRNA in underfed rats was significantly lower than in normal controls. Masseter muscle IGF-I Eb mRNA in severely underfed rats was significantly lower than in normal control and hypophysectomized rats. Soleus muscle myostatin mRNA in hypophysectomized rats was significantly higher than in normal and significantly underfed rats. No significant differences in plantaris and masseter muscle myostatin mRNA were observed between groups.. Suppressed muscle growth caused by hypophysectomy and underfeeding may be attributed mainly to reduced circulating IGF-I and partially to reduced IGF-I mRNA, rather than to a change in myostatin.

Topics: Animals; Animals, Newborn; Body Weight; Hypophysectomy; Insulin-Like Growth Factor I; Male; Malnutrition; Muscle, Skeletal; Myostatin; Rats; Rats, Wistar; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Transforming Growth Factor beta