Terveen miehen anabolisten steroidien käyttö

Testosteronin ja anabolisten steroidien käyttö on lisääntynyt kilpaurheilun ulkopuolella tavallisten kuntoiluharrastajien keskuudessa. Kuntodopingin käytöllä tavoitellaan muutoksia suorituskykyyn ja erityisesti ulkonäköön. Anabolisten steroidien käyttöön liittyy tunnettuja ja vakavia useisiin elinjärjestelmiin liittyviä haittavaikutuksia. Kuntodopingissa useiden anabolisten steroidivalmisteiden yhdistely suuriksi annoksiksi ja lisäksi muiden lääkeaineiden käyttö steroidien rinnalla lisäävät edelleen haittavaikutuksien esiintymistä. Yleisiä haittavaikutuksia miehillä ovat siittiötuotannon häiriö, hedelmättömyys ja anabolisten hormonien käyttöön liittyvä hypogonadismi, jotka tulisi tunnistaa. Suurimmalla osalla sekundaarinen hypogonadismi ja kivesten toiminta palautuvat kuukausien kuluessa anabolisten steroidien käytön lopettamisesta.</p

Addition of insulin glargine or NPH insulin to metformin monotherapy in poorly controlled type 2 diabetic patients decreases IGF-I bioactivity similarly

Aims/hypothesis The aim of this study was to compare IGFI bioactivity 36 weeks after the addition of insulin glargine (A21Gly,B31Arg,B32Arg human insulin) or NPH insulin to metformin therapy in type 2 diabetic patients who had poor glucose control under metformin monotherapy. Methods In the Lantus plus Metformin (LANMET) study, 110 poorly controlled insulin-naive type 2 diabetic patients were randomised to receive metformin with either insulin glargine (G+MET) or NPH insulin (NPH+MET). In the present study, IGF-I bioactivity was measured, retrospectively, in 104 out of the 110 initially included LANMET participants before and after 36 weeks of insulin therapy. IGF-I bioactivity was measured using an IGF-I kinase receptor activation assay. Results After 36 weeks of insulin therapy, insulin doses were comparable between the G+MET (68±5.7 U/day) and NPH+MET (71±6.2 U/day) groups (p=0.68). Before insulin therapy, circulating IGF-I bioactivity was similar between the G+MET (134±9 pmol/l) and NPH+MET (135 ±10 pmol/l) groups (p=0.83). After 36 weeks, IGF-I bioactivity had decreased significantly (p=0.001) and did not differ between the G+MET (116±9 pmol/l) and NPH+MET (117± 10 pmol/l) groups (p=0.91). At baseline and after insulin therapy, total IGF-I concentrations were comparable in both groups (baseline: G+MET 13.3±1.0 vs NPH+MET 13.3± 1.0 nmol/l, p=0.97; and 36 weeks: 13.4±1.0 vs 13.1± 0.9 nmol/l, p=0.71). Total IGF-I concentration did not change during insulin therapy (13.3±0.7 vs 13.3±0.7 nmol/l, baseline vs 36 weeks, p=0.86). Conclusions/interpretation Addition of insulin glargine or NPH insulin to metformin monotherapy in poorly controlled type 2 diabetic patients decreases serum IGF-I bioactivity in a similar manner

Liver fat and lipid oxidation in humans.

BACKGROUND: Studies in animals show that changes in hepatic fatty acid oxidation alter liver fat content. Human data regarding whole-body and hepatic lipid oxidation are controversial and based on studies of only a few subjects. AIMS: We examined whether whole-body and hepatic lipid oxidation are altered in subjects with non-alcoholic fatty liver disease (NAFLD) compared with controls. METHODS: In vivo measurements of rates of substrate oxidation and insulin sensitivity (using the euglycaemic hyperinsulinaemic clamp technique in combination with indirect calorimetry and infusion of [3-(3)H]glucose) were performed in subjects with NAFLD [mean liver fat 14.0% (interquartile range 7.5-20.5%), n=29] and in control subjects [1.6% (1.0-3.0%), n=29]. Liver fat was measured using proton magnetic resonance spectroscopy. Plasma concentrations of 3-hydroxybutyrate (3-OHB) were measured as markers of hepatic lipid oxidation. RESULTS: In the basal state, substrate oxidation rates and serum 3-OHB concentrations were comparable in subjects with and without NAFLD. Plasma 3-OHB concentrations were similarly suppressed by insulin in both the groups. During the insulin infusion, whole-body lipid oxidation was inversely correlated with insulin-stimulated glucose disposal (r=-0.48, P&lt;0.0001), which was lower in subjects with NAFLD [3.7+/-0.2 mg/(kg fat-free mass min)] than in the control subjects [5.0+/-0.3 mg/(kg fat-free mass min), P=0.0008]. CONCLUSIONS: Hepatic lipid oxidation is unchanged in NAFLD. Whole-body lipid oxidation is increased because of peripheral insulin resistance. These data imply that alterations in hepatic fatty acid oxidation do not contribute to liver fat content in humans