l-THYROXINE, CORTISOL AND DIET AFFECT THE LEVEL OF AMYLASE IN THE PAROTID GLAND OF DEVELOPING RATS

Kumegawa, Masayoshi; Maeda, Norihiko; Yajima, Toshihiko; Teratani, Takuma; Ikeda, Erika; Minamide, Chikage

doi:10.1677/joe.0.0870065

Cited by 13 publications

(6 citation statements)

References 18 publications

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“…Fetal serum corticosterone concentration is at the adult level during the last stage of gestation, rapidly declines after birth, and increases back to the adult level between 15 and 25 days of age (Takeuchi et al,1977a,1978). Maturation of the parotid acini, as assessd by α‐amylase per unit of tissue, is delayed when the postnatal rise in either thyroid or corticosteroid hormones are surgically or chemically prevented (Takeuchi et al,1977b) and precocious when either hormone is injected at 6 to 8 days of age (Sasaki et al,1976; Takeuchi et al1978; Takuma et al,1978; Kumegawa et al,1980). It should be noted that there are parallel effects on general development, e.g., eye opening and tooth eruption (Bakke et al,1975; Froelich and Meserve,1982; Gamborino et al,2001) that may influence parotid acinar maturation by means of early change from liquid to solid diet (Redman,1987).…”

Section: Discussionmentioning

confidence: 99%

Effects of Exogenous Thyroid Hormone on the Postnatal Morphogenesis of the Rat Parotid Gland

Ikeda

Aiyama

Redman³

2007

The Anatomical Record

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Administration of thyroid hormone has been shown to accelerate the early postnatal development of the rat parotid gland, but these studies have dwelt almost entirely on biochemical changes. The objective of this study was to describe the effects of exogenous thyroid hormone on morphologic aspects of the developing parotid gland, in particular the transient appearance of scattered mucous cells in this otherwise serous gland. Pups were given a daily subcutaneous injection of thyroxine (T(4)) of 0.1, 0.5, or 5.0 microg/g body weight, vehicle only (injection control), or no injection (normal control) beginning at 4 days, and killed for the collection of blood and parotid glands at intervals through 15 days. The serum was analyzed for T(4) and the glands were examined by light and electron microscopy. The results indicated that both serum T(4) and the pace of gland development were proportional to the dose of T(4). In particular, T(4) accelerated decreases in acinar size and gland area occupied by stroma and translocation of a subset of cells with small secretory granules, deeply stained with periodic acid-Schiff, from acini to intercalated ducts. However, the chronology of mucous cell disappearance was indifferent to treatment. In addition, signs of toxicity, including slower gain in body weight and greatly increased apoptosis and vacuoles in the glands, occurred with the higher doses of T(4).

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Section: Discussionmentioning

confidence: 99%

Effects of Exogenous Thyroid Hormone on the Postnatal Morphogenesis of the Rat Parotid Gland

Ikeda

Aiyama

Redman³

2007

The Anatomical Record

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“…In addition, exogenous thyroid hormone has been shown to induce precocious rises in serum corticosterone and corticosteroid-binding globulin in rat pups (D’Agostino and Henning 1982). Exogenous corticosteroids have been shown to increase the rate of other aspects of rat and mouse salivary gland differentiation (Johannessen 1965, Sasaki et al 1976, Takeuchi et al 1977a,b, Kumegawa et al 1980, Johnson 1987, Ikeda et al 2008, Inukai et al 2008). Thus, it is possible that a T 4 -induced rise in serum corticosteroids also may have been involved in the acceleration of MEC translocation and decline in parenchymal cell proliferative activity observed here.…”

Section: Discussionmentioning

confidence: 99%

“…This permits the study of factors that influence gland development via interventions applied directly to the pups, thus avoiding modifications of the effects of application via the dams. Alterations of diet and hormones have been shown to influence strongly postnatal development of rodent salivary glands (Sasaki et al 1976, Takeuchi et al 1977a,b 1978, Takuma et al 1978, Kumegawa et al 1980, Johnson 1987, Ikeda et al 2008, Inukai et al 2008). Serum thyroid hormone concentration is low in the perinatal rat, increases to twice the adult level by 16 days of age, and returns to the adult level by 30 days (Clos et al 1974, Porterfield and Hendrick 1981, Dussault et al 1982, Porterfield 1985, Farwell and Dubord-Tomasetti 1999).…”

mentioning

confidence: 99%

Exogenous thyroid hormone affects myoepithelium and proliferation in the developing rat parotid gland

Ikeda

Aiyama

Redman³

2010

Biotechnic & Histochemistry

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In the mature rat parotid gland, myoepithelial cells (MEC) invest intercalated ducts, but not acini. During postnatal development, however, these cells differentiate around both intercalated ducts and acini, then translocate to only intercalated ducts during weaning. Previously, we found that thyroxine (T4) accelerates translocation of cells with small secretory granules from acini into intercalated ducts and the number of apoptotic cells increased tremendously with high doses. We present here additional analysis of the effects of T4 on developing rat parotid gland, namely, the distribution of MEC and the proliferation of parenchymal cells. Beginning at age 4 days, pups were given daily subcutaneous injections of low, medium and high doses of T4 or vehicle or no injection. At ages 4, 7, 10 and 15 days, glands were excised and processed for light microscopy. Sections were double-immunostained with antibodies against proliferating cell nuclear antigen (PCNA) and actin, and counterstained with hematoxylin. Proliferative activity was assessed via PCNA histochemistry and MEC were identified using actin histochemistry. MEC in the T4 groups invested mostly acini at 15 days in vehicle/normal glands and mostly intercalated ducts after 10 days in the T4 groups. The proliferative activity of acinar cells and MEC in vehicle/normal glands declined progressively with age and T4 increased the rate of this decline in the MEC in a dose-dependent manner. We conclude that T4 accelerates the translocation of MEC from acini to intercalated ducts, with an important mechanism being the more rapid decline in the proliferative activity of MEC than in acinar cells in the T4 groups. Some of the decline in the proliferative activity of all cells in the high and medium dose T4 groups after 7 days may have been due to dose-related thyroxine toxicity.

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“…1). It was previously reported that administration of thyroxine at an early age results in an enhanced synthesis of amylase by the parotid gland (31). Thus, it could be hypothesized that an enhanced parotid amylase content could be responsible for an enhanced baseline amylase secretion in hyperthyroid animals.…”

Section: Discussionmentioning

confidence: 99%

Modulation by thyroid hormones of rat parotid amylase secretion stimulated by 5‐hydroxytryptamine

Ostuni

Houssay

Tumilasci

2003

European J Oral Sciences

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The effects of 5-hydroxytryptamine (5-HT) upon amylase secretion by rat parotid glands were studied in three groups of animals: (a) intact control rats (euthyroid rats); (b) hypothyroid rats obtained by surgical thyroidectomy 2 wk before the experiments; and (c) hyperthyroid rats obtained by the administration of sodium l-triiodothyronine for 2 wk before the experiments. Hyperthyroid rats showed significantly higher baseline amylase release than control rats. When the glands were stimulated with 5-HT (30 micro m), amylase release was significantly lower in the hypothyroid group and higher in the hyperthyroid rats than in control group. Addition of cholinergic, adrenergic or substance P antagonists did not modify 5-HT-stimulated amylase activity. The effects of 5-HT were partly but significantly blocked by the addition of 10 micro m methysergide (HT1/2/7 receptor blocker) in the three groups of rats. In contrast, 10 micro m ketanserine (HT2A receptor blocker) partly blocked the response to 5-HT only in the hyperthyroid animals. It was concluded that 5-HT induces amylase secretion by rat parotid glands through specific serotoninergic receptors, and that thyroid status modulates the 5-HT effect.

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l-THYROXINE, CORTISOL AND DIET AFFECT THE LEVEL OF AMYLASE IN THE PAROTID GLAND OF DEVELOPING RATS

Cited by 13 publications

References 18 publications

Effects of Exogenous Thyroid Hormone on the Postnatal Morphogenesis of the Rat Parotid Gland

Effects of Exogenous Thyroid Hormone on the Postnatal Morphogenesis of the Rat Parotid Gland

Exogenous thyroid hormone affects myoepithelium and proliferation in the developing rat parotid gland

Modulation by thyroid hormones of rat parotid amylase secretion stimulated by 5‐hydroxytryptamine

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