Thyroid hormones are involved in insulin-like growth factor-I (IGF-I) production by stimulating hepatic growth hormone receptor (GHR) gene expression in the chicken

Tsukada, Akira; Ohkubo, Tadayasu; Sakaguchi, Kesami; Tanaka, Minoru; Nakashima, Kenichiro; Hayashida, Yukinobu; Wakita, Masaaki; Hoshino, Sadao

doi:10.1016/s1096-6374(98)80116-0

Cited by 41 publications

(22 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…4 ). Earlier studies have shown that PTU-induced hypothyroidism depresses plasma IGF-1 levels (Cogburn et al, 1989a;Cogburn, 1991) and expression of GHR and IGF1 transcripts (Tsukada et al, 1998). Although not observed in the present study, depressed plasma levels of GH and IGF1 and consequently retarded growth have been demonstrated in T 3 -fed chickens (Cogburn et al, 1989a;Cogburn, 1991).…”

Section: Discussioncontrasting

confidence: 59%

Manipulation of thyroid status and/or GH injection alters hepatic gene expression in the juvenile chicken

Wang

Carré

Saxton

et al. 2007

Cytogenet Genome Res

View full text Add to dashboard Cite

Both thyroid hormone (T₃) and growth hormone (GH) are important regulators of somatic growth in birds and mammals. Although T₃-mediated gene transcription is well known, the molecular basis of T₃interaction with GH on growth and development of birds remains unknown. In earlier studies, we discovered that exogenous GH alone increased accumulation of visceral fat in young chickens, while the combination of GH injections and dietary T₃ worked synergistically to deplete body fat. In the present study, cDNA microarray and quantitative RT-PCR analyses enabled us to examine hepatic gene expression in young chickens after chronic manipulation of thyroid status and GH injection alone or in combination with T₃. Thyroid status modulates expression of common and unique sets of genes involved in a wide range of molecular functions (i.e., energy metabolism, storage and transport, signal transduction, protein turnover and drug detoxification). Hepatic expression of 35 genes was altered by hypothyroidism (e.g., ADFP, ANGPTL3, GSTΑ, CAT, PPARG, HMGCL, GHR, IGF1, STAT3, THRSPα), whereas hyperthyroidism affected expression of another cluster of 13 genes (e.g., IGFBP1, KHK, LDHB, BAIA2L1, SULT1B, TRIAD3). Several genes were identified which have not been previously ascribed as T₃ responsive (e.g., DEFB9, EPS8L2, ARHGAP1, LASS2, INHBC). Exogenous GH altered expression of 17 genes (e.g., CCAR1, CYP2C45, GYS2, ENOB, HK1, FABP1, SQLE, SOCS2, UPG2). The T₃+GH treatment depleted the greatest amount of body fat, where 34 differentially expressed genes were unique to this group (e.g., C/EBP, CDC42EP1, SYDE2, PCK2, PIK4CA, TH1L, GPT2, BHMT). The marked reduction in body fat brought about by the T₃+GH synergism could involve modulation of hormone signaling via altered activity of the Ras superfamily of molecular switches, which control diverse biological processes. In conclusion, this study provides the first global analysis of endocrine (T₃ and GH) regulation of hepatic gene transcription in the chicken.

show abstract

Section: Discussioncontrasting

confidence: 59%

Manipulation of thyroid status and/or GH injection alters hepatic gene expression in the juvenile chicken

Wang

Carré

Saxton

et al. 2007

Cytogenet Genome Res

View full text Add to dashboard Cite

show abstract

“…Hyperstaturism was described in our proband and bone was severely affected, indicating that, despite mild and unrecognized clinical symptoms, tissue thyrotoxicosis had been long-standing. Increased growth velocity was, at least in part, mediated by the thyroid hormonedependent induction of IGF-I secretion from the liver, perhaps through the stimulation of hepatic growth hormone receptor gene expression, as already seen in the chicken (23). Consistently, increased IGF-I secretion reverted to normal during MMI treatment.…”

Section: Discussionsupporting

confidence: 56%

A novel germline mutation in the TSH receptor gene causes non-autoimmune autosomal dominant hyperthyroidism

Alberti

Proverbio

Costagliola

et al. 2001

European Journal of Endocrinology

View full text Add to dashboard Cite

Objective: Clinical and genetic investigations were undertaken in a case of familial hyperthyroidism, with onset of thyrotoxic symptoms varying between childhood/adolescence. Methods: Automatic sequence analysis was carried out of the TSH receptor (TSHR) gene. Functional studies were undertaken of mutant TSHR in transient expression experiments in COS-7 cells including the evaluation of cAMP accumulation and of protein expression by¯ow cytometry, as well as the calculation of speci®c constitutive activity (SCA). Results: In four affected cases, the age of onset of thyrotoxic manifestations of non-autoimmune origin varied between 5 and 18 years. The disease transmission was typically autosomal dominant. TSHR gene sequence revealed the presence of a germline heterozygous substitution at codon 597 leading to the novel mutation V597F. This residue is located in the 5th transmembrane domain of the receptor protein in a critical region for membrane targeting and signal transduction. Functional studies of the V597F mutant indicate an 11-fold increase in SCA, associated with a reduction in receptor protein expression on the cytoplasmic membrane. Conclusions: Description was made of a family with non-autoimmune autosomal dominant hyperthyroidism carrying a novel mutation of TSHR leading to the increment in speci®c constitutive activity. Factors that may in¯uence the clinical expression of TSHR germline mutations are discussed.

show abstract

“…T 3 strongly potentiated the response to GH in rat hepatocyte culture (Tollet et al 1990), and both strongly potentiated the response to GH and induced GHR in pig hepatocyte culture (Brameld et al 1995). In hypothyroid chickens, thyroid hormone replacement normalized decreases in serum IGF-I, liver IGF-I mRNA, liver GHR mRNA and liver GH binding (Tsukada et al 1998). Thyroid hormones may be less important in the regulation of liver IGF-I production in fishes than in tetrapods.…”

Section: Discussionmentioning

confidence: 93%

Metabolic hormones modulate the effect of growth hormone (GH) on insulin-like growth factor-I (IGF-I) mRNA level in primary culture of salmon hepatocytes

Pierce

Fukada²,

Dickhoff³

2005

Journal of Endocrinology

View full text Add to dashboard Cite

Liver production of insulin-like growth factor-I (IGF-I) is a major point of control in the growth hormone (GH)/IGF axis, the endocrine system regulating body growth in fishes and other vertebrates. Pituitary GH stimulates hepatocyte production of IGF-I; however, in catabolic states, hepatocyte GH resistance results in decreases in liver IGF-I production. To investigate endocrine mechanisms leading to the development of hepatocyte GH resistance, we examined the regulation of IGF-I mRNA level by GH and metabolic hormones in primary culture of salmon hepatocytes. Cells were cultured in RPMI medium, and exposed to insulin (Ins, 10 6

show abstract

Thyroid hormones are involved in insulin-like growth factor-I (IGF-I) production by stimulating hepatic growth hormone receptor (GHR) gene expression in the chicken

Cited by 41 publications

References 33 publications

Manipulation of thyroid status and/or GH injection alters hepatic gene expression in the juvenile chicken

Manipulation of thyroid status and/or GH injection alters hepatic gene expression in the juvenile chicken

A novel germline mutation in the TSH receptor gene causes non-autoimmune autosomal dominant hyperthyroidism

Metabolic hormones modulate the effect of growth hormone (GH) on insulin-like growth factor-I (IGF-I) mRNA level in primary culture of salmon hepatocytes

Contact Info

Product

Resources

About