Endocrine and cardiac paracrine actions of insulin-like growth factor-I (IGF-I) during thyroid dysfunction in the rat: is IGF-I implicated in the mechanism of heart weight/body weight change during abnormal thyroid function?

Thomas, M; Miell, John P.; Taylor, Amy; Ross, R. J. M.; Arnao, J R; Jewitt, D E; McGregor, A. M.

doi:10.1677/jme.0.0100313

Cited by 28 publications

(17 citation statements)

References 30 publications

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“…Although hypothyroidism lowers circulating and liver IGF-I concentrations, hyperthyroidism does not seem to modify serum or hepatic levels of this hormone in male or non-pregnant rats (7,49,50). We also observed no significant modifications in liver mRNA concentration of IGF-I in virgin rats or during pregnancy, but the postpartum increase was advanced, perhaps reflecting the advancement in luteolysis and parturition (3).…”

Section: Discussionmentioning

confidence: 45%

Effect of chronic thyroxine treatment on IGF-I, IGF-II and IGF-binding protein expression in mammary gland and liver during pregnancy and early lactation in rats

Rosato

Lindenbergh-Kortleve

Neck

et al. 2002

European Journal of Endocrinology

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Objective: Hyperthyroidism in rats produces organ hypertrophy and increases in circulating IGF-I and IGF-binding protein (IGFBP)-3. Chronic treatment with thyroxine (T 4 ) during pregnancy advances parturition, blocks lactation and changes several hormone receptors in mammary gland and liver. Since IGFs are implicated in mammary and liver growth and in differentiation, we studied the effects of hyperthyroidism, induced by daily injections of T 4 (0.25 mg/kg). Design and Methods: Using quantitative RT-PCR and in situ hybridization, the gene expression of IGF-I, IGF-II and the IGFBPs was determined in mammary gland and liver of rats at estrus and days 7, 14 and 21 of pregnancy (G7, G14, G21), day 1 postpartum (L1) and 3 days after removing the litter (L4). Circulating levels of IGF-I, tri-iodothyronine (T 3 ), PRL and GH were measured. Results: T 4 treatment (HT) increased circulating T 3 save on G21, did not change serum IGF-I, increased PRL on G21 and decreased GH on L1. PRL decreased on L1 because of the absence of lactation. Hepatic IGF-I mRNA was low during pregnancy and increased on L4. HT advanced this increase to L1. In controls, liver IGFBP-3 mRNA levels decreased from G14 to G21, whereas IGFBP-4 showed an inverse pattern. HT lowered IGFBP-3 mRNA and increased IGFBP-4. Increases in mammary concentrations of IGF-I, IGFBP-3 and IGFBP-4 mRNAs were seen on G21. HT delayed these peaks to L1. Mammary IGF-II and IGFBP-2 mRNA levels were high on G7 and G14, and fell afterwards, with HT having no effects. IGFBP-5 mRNA decreased during pregnancy and increased on L1. HT increased IGFBP-5 levels in early pregnancy and on L1. IGF-I mRNA localized to connective and epithelial mammary tissue, while IGFBP-2 and IGFBP-5 mRNA was only in epithelial cells. Conclusion: These results imply a role for IGF-I, IGFBP-3 and IGFBP-4 in terminal mammary development, while IGF-II and IGFBP-2 may be implicated in early growth. IGFBP-5 has been implicated in mammary apoptosis, and the HT-induced increase may play a role in the premature mammary involution of the HT rats.

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Section: Discussionmentioning

confidence: 45%

Effect of chronic thyroxine treatment on IGF-I, IGF-II and IGF-binding protein expression in mammary gland and liver during pregnancy and early lactation in rats

Rosato

Lindenbergh-Kortleve

Neck

et al. 2002

European Journal of Endocrinology

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“…Methimazoleinduced hypothyroidism decreased circulating IGF-I levels in broilers (Decuypere et al 1987). Thomas et al (1993) reported similar serum IGF-I concentrations, but a 70% reduction in serum IGF-I bioactivity and reduced body weight in hyperthyroid rats compared with control animals. If such a reduction in bioactivity occurred in the present study, a reduction in skeletal muscle protein synthesis would be conceivable, despite no significant alteration in circulating, immunoassayable IGF-I concentrations.…”

Section: Gh-thyroid Axis Interactions: Consequences For Muscle Growthmentioning

confidence: 86%

Altered chicken thyroid hormone metabolism with chronic GH enhancement in vivo: consequences for skeletal muscle growth

Vasilatos‐Younken¹,

Zhou²,

Wang³

et al. 2000

Journal of Endocrinology

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In contrast to most vertebrates, GH reportedly has no effect upon somatic growth of the chicken. However, previous studies employed only one to two dosages of the hormone, and limited evidence exists of a hyperthyroid response that may confound its anabolic potential. This study evaluated the effects of 0, 10, 50, 100 and 200 µg/kg body weight per day chicken GH (cGH) (0-200 GH) infused i.v. for 7 days in a pulsatile pattern to immature, growing broiler chickens (9-10 birds/dosage). Comprehensive profiles of thyroid hormone metabolism and measures of somatic growth were obtained.Overall (average) body weight gain was reduced 25% by GH, with a curvilinear, dose-dependent decrease in skeletal (breast) muscle mass that was maximal (12%) at 100 GH. This profile mirrored GH dose-dependent decreases in hepatic type III deiodinase (DIII) activity and increases in plasma tri-iodothyronine (T 3 ), with both also maximal (74 and 108% respectively) at 100 GH. No effect on type I deiodinase was observed. At the maximally effective dosage, hepatic DIII gene expression was reduced 44% versus controls. Despite dose-dependent, fold-increases in hepatic IGF-I protein content, circulating IGF-I was not altered with GH infusion, suggesting impairment of hepatic IGF-I release. Significant, GH dose-dependent increases in plasma non-esterified fatty acid and glucose, and overall decreases in triacylglycerides were also observed. At 200 GH, feed intake was significantly reduced (19%; P<0·05) versus controls; however, additional control birds pair-fed to this level did not exhibit any responses observed for GH-treated birds.The results of this study support a pathway by which GH impacts on thyroid hormone metabolism beginning at a pretranslational level, with reduced hepatic DIII gene expression, translating to reduced protein (enzyme) expression, and reflected in a reduced level of peripheral T 3 -degrading activity. This contributes to decreased conversion of T 3 to its inactive form, thereby elevating circulating T 3 levels. The hyper-T 3 state leads to reduced net skeletal muscle deposition, and may impair release of GH-enhanced, hepatic IGF-I.In conclusion, GH has significant biological effects in the chicken, but profound metabolic actions predominate that may confound positive, IGF-I-mediated skeletal muscle growth.

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“…Ojamaa et al (1992) demonstrated that thyroid hormone upregulated the expression of the myosin heavy chain genes. Thomas et al (1993) showed that insulin-like growth factor-I produced cardiac hypertrophy, as well as endocrine and cardiac paracrine effects, during hyperthyroidism. Based on these previous literature reports, it seems likely that the animal model of hyperthyroidism-induced cardiac hypertrophy is in fact multi-factorial in its mechanistic nature.…”

Section: Discussionmentioning

confidence: 99%

Local renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy

Kobori¹,

Ichihara²,

Miyashita³

et al. 1999

Journal of Endocrinology

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We have reported previously that thyroid hormone activates the circulating and tissue renin-angiotensin systems without involving the sympathetic nervous system, which contributes to cardiac hypertrophy in hyperthyroidism. This study examined whether the circulating or tissue renin-angiotensin system plays the principal role in hyperthyroidism-induced cardiac hypertrophy. The circulating renin-angiotensin system in Sprague-Dawley rats was fixed by chronic angiotensin II infusion (40 ng/ min, 28 days) via mini-osmotic pumps. Daily i.p. injection of thyroxine (0·1 mg/kg per day, 28 days) was used to mimic hyperthyroidism. Serum free tri-iodothyronine, plasma renin activity, plasma angiotensin II, cardiac renin and cardiac angiotensin II were measured with RIAs. The cardiac expression of renin mRNA was evaluated by semiquantitative reverse transcriptase-polymerase chain reaction. Plasma renin activity and plasma angiotensin II were kept constant in the angiotensin II and angiotensin II+thyroxine groups (0·12 0·03 and 0·15 0·03 µg/h per liter, 126 5 and 130 5 ng/l respectively) (means ...). Despite stabilization of the circulating renin-angiotensin system, thyroid hormone induced cardiac hypertrophy (5·0 0·5 vs 3·5 0·1 mg/g) in conjunction with the increases in cardiac expression of renin mRNA, cardiac renin and cardiac angiotensin II (74 2 vs 48 2%, 6·5 0·8 vs 3·8 0·4 ng/h per g, 231 30 vs 149 2 pg/g respectively). These results indicate that the local renin-angiotensin system plays the primary role in the development of hyperthyroidism-induced cardiac hypertrophy.

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Endocrine and cardiac paracrine actions of insulin-like growth factor-I (IGF-I) during thyroid dysfunction in the rat: is IGF-I implicated in the mechanism of heart weight/body weight change during abnormal thyroid function?

Cited by 28 publications

References 30 publications

Effect of chronic thyroxine treatment on IGF-I, IGF-II and IGF-binding protein expression in mammary gland and liver during pregnancy and early lactation in rats

Effect of chronic thyroxine treatment on IGF-I, IGF-II and IGF-binding protein expression in mammary gland and liver during pregnancy and early lactation in rats

Altered chicken thyroid hormone metabolism with chronic GH enhancement in vivo: consequences for skeletal muscle growth

Local renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy

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