Effect of experimental hyperthyroidism on skeletal-muscle proteolysis

Carter, W J; Benjamin, Wieke S. van der Weijden; Faas, Fred H.

doi:10.1042/bj1940685

Cited by 47 publications

(22 citation statements)

References 13 publications

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“…One possible mechanism is increased proteolysis induced by the hyperthyroidism, which has been previously demonstrated in a rat model. 18 Previous studies have shown other skeletal muscle dysfunction in human beings with hyperthyroidism secondary to Graves disease. 19 This finding was thought to be the result of elevated levels of thyroid hormone and circulating catecholamines.…”

Section: Discussionmentioning

confidence: 97%

Effect of Hyperthyroidism on the Orbicularis Oculi Muscle in Rabbits

Harrison

McLoon

2002

Ophthalmic Plastic & Reconstructive Surgery

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Purpose:To determine the effect of hyperthyroidism on both myofiber number and myosin heavy-chain isoform composition within the palpebral orbicularis oculi muscle in rabbits.Methods: Four New Zealand White rabbits were made hyperthyroid by injection of 3,3,3'-triiodothyroinine intraperitoneally every other day for 1 month. Four rabbits were used as control animals. After 1 month the rabbits were euthanized, and the eyelids were excised and sectioned in a cryostat. The sections were immunostained to determine the presence of fast, slow, and neonatal myosin heavy-chain isoforms. To determine alterations in myofiber number, differential counts of myofiber number and the cross-sectional areas of the muscle fibers were performed with the use of computerized morphometry.Results: The orbicularis oculi muscle in the palpebral portion of the eyelids from hyperthyroid rabbits had significantly fewer myofibers compared with control eyelids, predominantly as the result of a loss of myofibers in the preseptal region. The remaining fibers showed continued expression of fast myosin but upregulated coexpression of slow myosin isoform.Conclusions: Hyperthyroidism led to reduced orbicularis oculi muscle in the rabbit model and an alteration in the myosin heavy-chain isoform composition. This finding may help explain the clinical finding of eyelid retraction in patients with Graves orbitopathy.Graves disease is an autoimmune process often associated with an endocrinopathy that leads to an inflammatory orbitopathy with proptosis, strabismus, and eyelid retraction.1,2 The histologic changes in the extraocular muscles, orbital fat, levator superioris, and the Müller muscle have been well described. [3][4][5] To the best of our knowledge, no prior histologic studies have examined the effects of hyperthyroidism on the orbicularis oculi muscle. The current study begins to fill that void.There is no satisfactory animal model for the autoimmune process that leads to Graves disease. Although hyperthyroidism is not always associated with Graves ophthalmopathy, its frequent association lends credibility to the study of the effects of hyperthyroidism on the ocular and nonocular skeletal muscles in other species. A number of studies have been performed with animal models of elevated thyroid hormone to study various muscle-specific aspects caused by this condition. 6 -15 The purpose of this study was to evaluate the effect of elevated thyroid hormone levels on orbicularis oculi muscle in a rabbit model.

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Section: Discussionmentioning

confidence: 97%

Effect of Hyperthyroidism on the Orbicularis Oculi Muscle in Rabbits

Harrison

McLoon

2002

Ophthalmic Plastic & Reconstructive Surgery

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“…However, even Rennis and Millward [29] agreed that urinary 3-MH can give a reliable description of changes in muscle protein breakdown under certain cir cumstances, i.e., when synchronous and par allel changes in 3-MH excretion and skeletal muscle protein breakdown occur. In a pre vious study, urinary excretion of 3-MH in creased by about 30% during experimental hyperthyroidism in rats concomitant with a similar relative increase in proteolytic rate in isolated epitrochlearis muscle [8], Thus, the increased 3-MH excretion following admin istration o fT 3 to rats may reflect accelerated skeletal muscle protein breakdown. This in terpretation was further supported by the re sults in a recent study from our laboratory in which protein degradation in soleus muscle of rats was increased by about 40% following T3 treatment for 3 days [3], Surgical trauma, especially when involv ing the gastrointestinal tract, may induce dis proportionate injury to 3-MH-containing tis sues, temporarily enhancing'3-MH produc tion from non-muscle sources.…”

Section: Discussionmentioning

confidence: 99%

“…Accel erated breakdown of muscle protein might be one factor in the development of muscle weakness and wasting commonly observed in hyperthyroid patients [27,31]. Urinary ex cretion of 3-methylhistidine (3-MH), which is often used as an index of skeletal muscle proteolysis [4,35], was increased both in experimental [7,8] and clinical hyperthy roidism [33].…”

Section: Introductionmentioning

confidence: 99%

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Effects of Beta-Blocking Agents on Urinary Excretion of 3-Methylhistidine during Experimental Hyperthyroidism in Rats

Angerås¹,

Jagenburg²,

Lindstedt³

et al. 1987

Eur Surg Res

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Beta-blocking agents are increasingly used as preoperative treatment of hyper-thyroid patients. Relatively little is known about the effects of these drugs on metabolic alterations in hyperthyroidism. The aim of this investigation was to study the effects of two different beta-blocking agents on the urinary excretion of 3-methylhistidine (3-MH) during experimental hyperthyroidism in rats. Experimental hyperthyroidism was induced by daily intraperitoneal injections of triiodothyronine (T₃; 100 µg/l00 g body weight) for 3 days. Control animals were injected with corresponding volumes of solvent. Groups of rats received food enriched with metoprolol (8.8 mmol/kg of diet) or propranolol (3.3 mmol/kg of diet) or food without additions. Urinary 3-MH excretion was increased by about 40% during experimental hyperthyroidism. A similar increase of 3-MH excretion was found in animals receiving T₃ + metoprolol, whereas the excretion of 3-MH was reduced to control level in hyper-thyroid rats receiving propranolol. No effects of metoprolol or propranolol on 3-MH excretion were found in control animals. Although the source of 3-MH cannot be exactly defined, the present results indicate that increased proteolysis in skeletal muscle and/or other tissues during experimental hyperthyroidism was reduced by propranolol.

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“…1) Hormonal stimuli, such as angiotensin II, endothelins, norepinephrine, and thyroid hormone, have also been postulated to play a role in the regulation of cardiac cell growh. [2][3][4][5] Based on the finding that angiotensin II stimulates protein synthesis of cardiac myocytes 6) and that angiotensin-converting enzyme (ACE) inhibitor induces regression of cardiac hypertrophy both in experimental animal models 7) and in hypertensive patients, 8) several studies have suggested a crucial role of the renin-angiotensin system locally present in the cardiac tissue in the formation of hypertrophy. 9) Indeed, the activation of the cardiac renin-angiotensin system, such as the upregulation of angiotensinogen, ACE and angiotensin II type-1 (AT1) receptor mRNAs, have been demonstrated in association with cardiac hypertrophy.…”

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confidence: 99%

Expressions of Bradykinin B2-Receptor, Kallikrein and Kininogen mRNAs in the Heart Are Altered in Pressure-Overload Cardiac Hypertrophy in Mice.

Yayama

Hiyoshi

Okamoto

2001

Biological & Pharmaceutical Bulletin

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Cardiac left ventricular hypertrophy is most commonly associated with hypertension and is an independent risk factor for cardiovascular events in patients with hypertension. Mechanical load or stretching in cardiac tissue has been identified as a growth stimulus and may be relevant in hypertension-induced cardiac hypertrophy.1) Hormonal stimuli, such as angiotensin II, endothelins, norepinephrine, and thyroid hormone, have also been postulated to play a role in the regulation of cardiac cell growh.2-5) Based on the finding that angiotensin II stimulates protein synthesis of cardiac myocytes 6) and that angiotensin-converting enzyme (ACE) inhibitor induces regression of cardiac hypertrophy both in experimental animal models 7) and in hypertensive patients, 8) several studies have suggested a crucial role of the renin-angiotensin system locally present in the cardiac tissue in the formation of hypertrophy. 9) Indeed, the activation of the cardiac renin-angiotensin system, such as the upregulation of angiotensinogen, ACE and angiotensin II type-1 (AT1) receptor mRNAs, have been demonstrated in association with cardiac hypertrophy. [10][11][12][13] In contrast to angiotensin II, kinins produced by the kallikrein-kinin system have been postulated to participate in the beneficial effects of ACE inhibitors, because ACE inhibitors prevent the degradation of kinins into inactive peptides by inhibiting kininase II, and B2 receptor antagonist abolished the reduction of cardiac hypertrophy by an ACE inhibitor in the rat aortic-banding model. 14,15) Kinins are released from high-and low-molecular-weight kininogens (H-and L-kininogens, respectively) by kininogenases such as plasma and tissue kallikreins.16) Evidence suggests that a local kallikrein-kinin system exists in the heart, which enables it to synthesize and release kinins. 17) In this respect, we have demonstrated that rat cardiac myocytes express mRNAs for bradykinin B2-receptor, kininogen and kallikrein, supporting the presence of the local kallikreinkinin system in the heart. 18) Recent studies have provided evidence that kinins released locally in the heart may act as autocrine/paracrine hormones, inhibiting the cardiac remodeling process, such as cardiomyocyte hypertrophy and hyperplasia of interstitial fibroblasts, suggesting that kinins are cardioprotective factors inhibiting the progression of cardiac hypertrophy. [19][20][21][22] In these studies, however, alterations of the cardiac kallikrein-kinin system during the formation of hypertrophy were not investigated. We hypothesized that the cardiac kallikrein-kinin system may be altered during the development of heart failure and may contribute to the pathophysiology of this disease state. Therefore, the present study was designed to answer this question by determining mRNA levels of the kallikrein-kinin components, such as kininogens, tissue kallikrein and bradykinin receptors, during the development of pressure-overload cardiac hypertrophy in mice. MATERIALS AND METHODSAbdominal Aorta Constriction Adult male...

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Effect of experimental hyperthyroidism on skeletal-muscle proteolysis

Cited by 47 publications

References 13 publications

Effect of Hyperthyroidism on the Orbicularis Oculi Muscle in Rabbits

Effect of Hyperthyroidism on the Orbicularis Oculi Muscle in Rabbits

Effects of Beta-Blocking Agents on Urinary Excretion of 3-Methylhistidine during Experimental Hyperthyroidism in Rats

Expressions of Bradykinin B2-Receptor, Kallikrein and Kininogen mRNAs in the Heart Are Altered in Pressure-Overload Cardiac Hypertrophy in Mice.

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