leptin and Congenital-Hypothyroidism

Topics: Adipose Tissue, Brown; Adipose Tissue, White; Animals; Congenital Hypothyroidism; Disease Models, Animal; Female; Insulin; Leptin; PPAR gamma; Sheep; Signal Transduction; Thermogenesis; Transcriptome; Uncoupling Protein 1

Thyroid hormone deficiency during crucial stages of development causes congenital hypothyroidism. This syndrome alters hypothalamic pathways involved in long-term bodyweight regulation as ObRb-STAT3 leptin signaling pathway, which is associated with metabolic syndrome. This study aimed to determine if thyroxine treatment during pregnancy and lactation in hypothyroid mothers avoids, in the congenital hypothyroid offspring, the alterations in metabolic programming related to metabolic syndrome and the ObRb-STAT3 leptin signaling pathway in hypothalamus. Twenty-four virgin female Wistar rats were divided into euthyroid, hypothyroid, and hypothyroid with thyroxine treatment (20 μg/kg/day T

Topics: Animals; Animals, Newborn; Congenital Hypothyroidism; Female; Gene Expression Regulation; Leptin; Male; Rats; Rats, Wistar; Receptors, Leptin; Signal Transduction; STAT3 Transcription Factor; Thyroxine

The goal of this study is to investigate whether congenital hypothyroidism induced by MMI during gestation (G) or gestation plus lactation (GL) would affect the leptin action upon body weight control on hypothalamus. Six to eight pups per group were killed at 90 days of age. For statistical analysis one-way ANOVA followed by the Holm-Sìdak post hoc test was used. Hypothyroidism resulted in a significant increase in leptin serum levels in G 20% and GL 25% (p<0.04). There was a significant expression decrease of OBR in G 45% and GL 63%; pSTAT3 in G 56% and GL 51%; pERK in G 50% and GL 48%; POMC in G 41% and GL 46% (p<0.04), while a significant increase was assigned to SOCS3 in G 52% and GL 170% (p<0.04) protein expression. We can conclude that hypothyroxinemia condition in rats on adulthood results in impairment of the leptin signaling pathway via ObRb-STAT3 in the hypothalamus, which is likely to be involved in the leptin resistance.

Topics: Aging; Animals; Body Weight; Congenital Hypothyroidism; Feeding Behavior; Female; Hormones; Hypothalamus; Leptin; Male; Rats, Wistar; Signal Transduction

Because leptin decreases food intake and increases energy expenditure, the possible influence of thyroid status on the leptin system has been investigated mainly in adults and animals. However, the data available at present are very confusing. The aim of the present study was to assess the possible interaction of thyroid hormones with the leptin system.. Serum free thyroxine (FT4), a biologically active thyroid hormone, and thyroid stimulating hormone (TSH), a sensitive and reliable index of thyroid status, were examined in 51 children (19 males, 32 females) with mass screening-detected congenital hypothyroidism on continuous L-thyroxine (L-T4) substitution therapy. The subjects were divided into younger (n = 35, aged 1 month-5 years) and older (n = 16, 6 years-11 years) children groups. Serum levels of leptin and thyroid hormones were measured in the subjects. Body mass index (BMI) was estimated by the formula bodyweight (kg)/height x height (m2), which is known as the Kaup index in younger children and BMI in older children and adults.. In the younger children group, serum leptin levels showed no correlation with serum TSH, FT4 or T4. In the older children group, serum leptin concentrations significantly correlated with T4 (r = 0.510, P < 0.05) and BMI (n = 16, r = 0.647, P < 0.01), but not with TSH or FT4.. The role of thyroid hormones in modulating leptin synthesis and secretion seems to have little, if any, clinical or biological relevance.

Topics: Body Mass Index; Child; Child, Preschool; Congenital Hypothyroidism; Female; Humans; Hypothyroidism; Infant; Leptin; Male; Mass Screening; Thyroid Hormones; Thyrotropin; Thyroxine