Thyroid Hormone Increases mRNA and Protein Expression of Na+-K+-ATPase α2 and β1 Subunits in Human Skeletal Muscles

Phakdeekitcharoen, Bunyong; Phudhichareonrat, Suchart; Pookarnjanamorakot, Chathchai; Kijkunasathian, Chusak; Tubtong, Nattha; Kittikanokrat, Wassana; Radinahamed, Piyanuch

doi:10.1210/jc.2006-0552

Cited by 13 publications

(19 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These findings are consistent with the improved insulin sensitivity reported in developmental GHD and GH insensitive (GHRKO) mice [19]–[21], but are in contrast to the majority of clinical studies showing adults with GHD are insulin resistant [22]–[24]. These apparent species differences may be more related to diet, lifestyle, environmental factors and/or etiology and specificity of GHD, based on the finding that a rural Brazilian family with isolated GHD due to an inactivating mutation in the GHRH-R, were also found to be more insulin sensitive, as compared to their normal counterparts [25], [26]. In addition adult patients with Laron syndrome (inactivating mutations in the GH receptor) remained relatively insulin sensitive (calculated by HOMA-IR), despite an obese phenotype [27].…”

Section: Discussionmentioning

confidence: 95%

Metabolic Impact of Adult-Onset, Isolated, Growth Hormone Deficiency (AOiGHD) Due to Destruction of Pituitary Somatotropes

Luque

Córdoba-Chacón

et al. 2011

PLoS ONE

View full text Add to dashboard Cite

Growth hormone (GH) inhibits fat accumulation and promotes protein accretion, therefore the fall in GH observed with weight gain and normal aging may contribute to metabolic dysfunction. To directly test this hypothesis a novel mouse model of adult onset-isolated GH deficiency (AOiGHD) was generated by cross breeding rat GH promoter-driven Cre recombinase mice (Cre) with inducible diphtheria toxin receptor mice (iDTR) and treating adult Cre+/−,iDTR+/− offspring with DT to selectively destroy the somatotrope population of the anterior pituitary gland, leading to a reduction in circulating GH and IGF-I levels. DT-treated Cre−/−,iDTR+/− mice were used as GH-intact controls. AOiGHD improved whole body insulin sensitivity in both low-fat and high-fat fed mice. Consistent with improved insulin sensitivity, indirect calorimetry revealed AOiGHD mice preferentially utilized carbohydrates for energy metabolism, as compared to GH-intact controls. In high-fat, but not low-fat fed AOiGHD mice, fat mass increased, hepatic lipids decreased and glucose clearance and insulin output were impaired. These results suggest the age-related decline in GH helps to preserve systemic insulin sensitivity, and in the context of moderate caloric intake, prevents the deterioration in metabolic function. However, in the context of excess caloric intake, low GH leads to impaired insulin output, and thereby could contribute to the development of diabetes.

show abstract

Section: Discussionmentioning

confidence: 95%

Metabolic Impact of Adult-Onset, Isolated, Growth Hormone Deficiency (AOiGHD) Due to Destruction of Pituitary Somatotropes

Luque

Córdoba-Chacón

et al. 2011

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…A clinical study had revealed that the symptoms of TPP would be relieved after control of hyperthyroidism [15]. Thyroid hormone can stimulate Na + /K + -ATPase expression in skeletal muscle [16]. Moreover, excessive thyroxine supplement in a hypopituitarism patient after surgical treatment of craniopharyngioma could lead to periodic paralysis [17], indicating that high thyroid hormone levels can lead to TPP.…”

Section: Discussionmentioning

confidence: 99%

Effects of sex steroid hormones, thyroid hormone levels, and insulin regulation on thyrotoxic periodic paralysis in Chinese men

Chen

Jiangfang

et al. 2010

Endocr

View full text Add to dashboard Cite

Our study is to determine the expression of thyroid hormone, sex hormone, insulin, and C-peptide in Chinese male patients with thyrotoxic periodic paralysis (TPP). This study covered 102 patients with hyperthyroidism from Xijing Hospital. According to whether occurrence of TPP or not, patients were divided into two groups (those that were hyperthyroid with and without TPP) that were, matched with age, blood pressure, urea, and creatinine. We found the body mass index (BMI) in patients with TPP was higher than that in pure hyperthyroidism patients. The levels of the total thyroxine (T4), free triiodothyronine (FT3), and free thyroxine (FT4) were significantly lower in patients with TPP compared with pure hyperthyroidism patients, while serum testosterone levels were higher compared with pure hyperthyroidism patients. Moreover, after glucose administration, the concentration of insulin at 60, 120, and 180 min were significantly higher in patients with TPP than those in pure hyperthyroidism patients. The insulin area under the curve (AUC) was significantly increased in patients with TPP compared with pure hyperthyroidism patients. The levels of thyroid hormone, sex hormone, and insulin were different in Chinese male patients with TPP compared to those with only hyperthyroidism.

show abstract

“…34,35 Thyroid response element (TRE) is present in some but not all isoforms of Na + , K + -ATPase subunits, and the stimulation by thyroid hormones may involve transcriptional as well as post-transcriptional mechanisms. 36,37 In general, the abundance of Na + , K + -ATPase is in good correlation with serum thyroid hormone levels.…”

Section: Na+ K+-atpase and Extracellular Potassium Homeostasismentioning

confidence: 99%

“…36,37 In general, the abundance of Na + , K + -ATPase is in good correlation with serum thyroid hormone levels. 35,38 …”

Section: Na+ K+-atpase and Extracellular Potassium Homeostasismentioning

confidence: 99%

Extracellular Potassium Homeostasis: Insights from Hypokalemic Periodic Paralysis

Cheng

Kuo

Huang

2013

Seminars in Nephrology

View full text Add to dashboard Cite

The extracellular potassium makes up only about 2% of the total body potassium store. The majority of the body potassium is distributed in the intracellular space, and of which about 80% is in skeletal muscle. Movement of potassium in and out of skeletal muscle thus plays a pivotal role in extracellular potassium homeostasis. The exchange of potassium between the extracellular space and skeletal muscle is mediated by specific membrane transporters. These include potassium uptake by Na+, K+-ATPase and release by inward rectifier K+ channels. These processes are regulated by circulating hormones, peptides, ions, and by physical activity of muscle as well as dietary potassium intake. Pharmaceutical agents, poisons and disease conditions also affect the exchange and alter extracellular potassium concentration. Here, we review extracellular potassium homeostasis focusing on factors and conditions that influence the balance of potassium movement in skeletal muscle. Recent findings that mutations of a skeletal muscle-specific inward rectifier K+ channel cause hypokalemic periodic paralysis provide interesting insights into the role of skeletal muscle in extracellular potassium homeostasis. These recent findings will be reviewed.

show abstract

Thyroid Hormone Increases mRNA and Protein Expression of Na+-K+-ATPase α2 and β1 Subunits in Human Skeletal Muscles

Abstract: This provides the first evidence that, in human skeletal muscles, thyroid hormone up-regulates the Na+-K+-ATPase protein expression at least, in part, at mRNA level, and the alpha2 and beta1 subunits play the important role in this regulation.

Cited by 13 publications

References 25 publications

Metabolic Impact of Adult-Onset, Isolated, Growth Hormone Deficiency (AOiGHD) Due to Destruction of Pituitary Somatotropes

Metabolic Impact of Adult-Onset, Isolated, Growth Hormone Deficiency (AOiGHD) Due to Destruction of Pituitary Somatotropes

Effects of sex steroid hormones, thyroid hormone levels, and insulin regulation on thyrotoxic periodic paralysis in Chinese men

Extracellular Potassium Homeostasis: Insights from Hypokalemic Periodic Paralysis

Contact Info

Product

Resources

About