Regulation of adiponectin gene expression in adipose tissue by thyroid hormones

Abstract

Available experimental data suggest that adiponectin and thyroid hormones have biological interaction in vivo. However, the effects of thyroid hormones on adipose adiponectin gene expression in thyroid dysfunction are unclear. We induced hyper- (HYPER) and hypothyroidism (HYPO) by daily administration of a 12 mg/l of levothyroxine and 250 mg/l of methimazole in drinking water of rats, respectively, for 42 days. The white adipose tissues and serum sample were taken on days 15, 28, 42 and also 2 weeks after treatment cessation. Analysis of adiponectin gene expression was performed by real-time PCR and 2(-ΔΔct) method. The levels of adipose tissue adiponectin mRNA in the HYPO rats were decreased during the 6-week treatment when compared to control rats (<0.05) and were increased significantly 2 weeks after HYPO cessation (P < 0.05). This decline in adiponectin gene expression occurred in parallel with a decrease in T3, T4, fT3 and fT4 concentrations (P < 0.05). In opposite to HYPO rats, adipose adiponectin gene expression was increased in HYPER rats during the 6-week treatment in parallel with an increase the thyroid hormones concentrations (P < 0.05), and its expression was decreased 2 weeks after HYPER cessation (P < 0.05). Adiponectin gene expression levels showed significant negative correlations with concentrations of LDL (HYPO; r = -0.806, P = 0.001 and HYPER; r = -0.749, P = 0.002), triglyceride (HYPO; r = -0.825, P = 0.001 and HYPER; r = -0.824, P = 0.001) and significant positive correlations with concentrations of glucose (HYPO; r = 0.674, P = 0.004 and HYPER; r = 0.866, P = 0.001) and HDL (HYPO; r = 0.755, P = 0.001 and HYPER; r = 0.839, P = 0.001). The current study provides evidence that adiponectin gene expression in adipose tissue is regulated by thyroid hormones at the translation level and that lipid and carbohydrate disturbances in a patient with thyroid dysfunction may be, in part, due to adiponectin gene expression changes.

Endocrine effects of tobacco smoke exposure during lactation in weaned and adult male offspring

“…The hyperthyroid status of the SE group can be partially explained by hyperleptinemia as leptin has a well-known stimulatory action on the thyroid axis (Casanueva & Dieguez 1999, Nowak et al 2002, Ortiga-Carvalho et al 2002, de Oliveira et al 2007. There is also an association between hyperthyroidism and hyperadiponectinemia (Yaturu et al 2004, Seifi et al 2012, which could help to explain the present findings in adult SE rats. Even without ever having smoked, adults or adolescents exposed to environmental tobacco smoke have a higher risk of developing cardiometabolic diseases (Weitzman et al 2005, Venn & Britton 2007, Xie et al 2010.…”

Serum Adiponectin Levels and Changes in Glucose Metabolism before and after Treatment for Thyroid Dysfunction

“…One possible explanation involves the induction of TSH receptors on adipose cells via the effects of TSH-stimulating antibodies, thus resulting in increased adiponectin production (38). Direct stimulation of adiponectin by thyroid hormones through the peroxisome proliferator-activated receptor (PPAR) signaling pathway is another hypothesis (39,40). Other proposed mechanisms include an increase in the number of adrenergic receptors and enhanced lipolysis in addition to an increased number of small adipocytes responsible for adiponectin production (41,42).…”

Effects of thyroxine treatment during lactation on the testicular function of rats across different ages

“…The reduction of body weight observed in treated rats can also result from an increase in circulating adiponectin [16,17]. Adiponectin increases insulin sensitivity by increasing fat oxidation resulting in a reduced body mass index [17] or a decrease in food intake of rats at weaning [15].…”

“…After birth, the immature Sertoli cells continue to proliferate until the beginning of puberty. At [15][16][17][18][19][20] th day after birth in rats, the cells stop dividing and start differentiating into their non-proliferative adult form [17,18]. Sertoli cells provide growth factors and nutrients for developing germ cells.…”