Supplementation with myo-inositol and Selenium improves the clinical conditions and biochemical features of women with or at risk for subclinical hypothyroidism.

Purpose: The present study aims to evaluate the effect of myo-Inositol plus Selenium supplementation in patients affected by subclinical hypothyroidism. Methods: One hundred and forty-eight patients were included in the study from 8 different centers of Slovakia, and treated for 6 months with a daily dose of 600 mg myo-Ins plus 83 mcg Se. The patients included at the enrollment were women of reproductive age (18-50), who exhibit values of TSH in the range 2.5-5 mU/l and positivity to antibodies TPO-Ab/TG-Ab, or otherwise values of TSH in the range 5-10 mU/l both with and without positivity to antibodies TPO-Ab/TG-Ab. Results: Patients affected by subclinical hypothyroidism exhibited a significant improvement of their condition when treated for 6 months with a combination of myo-Inositol and Selenium. The TSH values significantly ameliorated along with the index of autoimmunity and the thyroid status. In a sub-class of patients, the auto-antibody titer decreased after myo-inositol + Selenium administration. The treatment also induces a regularization of the menstrual cycle and a reduction of the cholesterol in the patients enrolled for the study. Furthermore, a significant improvement is observed in the perception of the symptoms associated with subclinical hypothyroidism over the treatment period. Conclusion: A dietary supplementation with of myo-Inositol and Selenium in the treatment of patients affected by subclinical hypothyroidism exhibits a beneficial role in the recovery of TSH values, in the improvement of the symptoms associated to this condition and in the maintenance of the thyroid functions.The trial was approved by the Ethical Committee from National Institute of Endocrinology and Diabetology of Lubochna, Slovakia, date 18.12.2018, registration number: 3124/2018.

Improved adipose tissue metabolism after 5-year growth hormone replacement therapy in growth hormone deficient adults: The role of zinc-α2-glycoprotein.

Growth hormone (GH) supplementation therapy to adults with GH deficiency has beneficial effects on adipose tissue lipid metabolism, improving thus adipocyte functional morphology and insulin sensitivity. However, molecular nature of these effects remains unclear. We therefore tested the hypothesis that lipid-mobilizing adipokine zinc-α2-glycoprotein is causally linked to GH effects on adipose tissue lipid metabolism. Seventeen patients with severe GH deficiency examined before and after the 5-year GH replacement therapy were compared with age-, gender- and BMI-matched healthy controls. Euglycemic hyperinsulinemic clamp was used to assess whole-body and adipose tissue-specific insulin sensitivity. Glucose tolerance was determined by oGTT, visceral and subcutaneous abdominal adiposity by MRI, adipocyte size morphometrically after collagenase digestion, lipid accumulation and release was studied in differentiated human primary adipocytes in association with GH treatment and zinc-α2-glycoprotein gene silencing. Five-year GH replacement therapy improved glucose tolerance, adipose tissue insulin sensitivity and reduced adipocyte size without affecting adiposity and whole-body insulin sensitivity. Adipose tissue zinc-α2-glycoprotein expression was positively associated with whole-body and adipose tissue insulin sensitivity and negatively with adipocyte size. GH treatment to adipocytes in vitro increased zinc-α2-glycoprotein expression (>50%) and was paralleled by enhanced lipolysis and decreased triglyceride accumulation (>35%). Moreover, GH treatment improved antilipolytic action of insulin in cultured adipocytes. Most importantly, silencing zinc-α2-glycoprotein eliminated all of the GH effects on adipocyte lipid metabolism. Effects of 5-year GH supplementation therapy on adipose tissue lipid metabolism and insulin sensitivity are associated with zinc-α2-glycoprotein. Presence of this adipokine is required for the GH action on adipocyte lipid metabolism in vitro.