Levels of Prolactin, Growth Hormone and Insulin in Genetically Diabetic (db/db) Mice

Sinha, Y. N.; Baxter, S. R.; Larson, B. A.; Vanderlaan, W. P.

doi:10.3181/00379727-161-40494

Cited by 17 publications

(6 citation statements)

References 8 publications

(10 reference statements)

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“…The stimulatory effect of estrogen on hepatic PRLR may be mediated, at least in part, by the hypothalamus-hypophyseal system, since estrogen is incapable of increasing the level of PRLR in hypophysectomized rats (Norstedt & Mode 1982) and pituitary PRL is able to up-regulate its own receptor (Manni et al 1978). In female diabetic mice, the levels of PRL in orbitally collected sera were lower than normal until 12 weeks of age, and thereafter the levels increased to normal levels (Sinha et al 1979). These results are consistent with our findings of the changes of hepatic PRLR mRNA in diabetic female mice during the postnatal period.…”

Section: Discussionmentioning

confidence: 99%

Involvement of gonadal steroid hormone disturbance in altered prolactin receptor gene expression in the liver of diabetic mice

Murakami¹,

Maeda²,

Oka³

1999

Journal of Endocrinology

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The levels of mRNA for long and three short forms of prolactin receptor (PRLR) were examined in the livers of normal (db+/db ) and insulin-resistant diabetic (db+/ db+) mice to assess the role of gonadal steroid hormones in the regulation of PRLR gene expression in diabetes mellitus. In females, plasma levels of testosterone in diabetic mice were higher, and those of 17 -estradiol were lower when compared with levels in normal mice. By contrast, diabetic male mice had lower plasma levels of testosterone than normal males and showed no significant difference in the low circulating level of 17 -estradiol compared with normal males. The short 3 form of PRLR (PRLR3) mRNA was the most abundant in the liver of both normal and diabetic mice. In addition, the level of PRLR3 mRNA in normal females was 8-fold higher than in normal males. The level of PRLR3 mRNA in diabetic females was approximately a quarter lower than in normal females, whereas the level of PRLR3 mRNA in diabetic males was approximately 2-fold higher than in normal males. During postnatal development, the level of PRLR3 mRNA increased during puberty in normal females, while the level in diabetic females decreased to a nadir at 7 weeks of age followed by a progressive rise. On the other hand, the levels of PRLR3 mRNA in both normal and diabetic males decreased gradually during 5 to 14 weeks of age. Testosterone treatment of diabetic males and females resulted in a 49·1 and 49·8% decrease of PRLR3 mRNA respectively. 17 -Estradiol treatment slightly (18%) increased levels of PRLR3 mRNA in diabetic males. These results suggest that the hepatic level of PRLR mRNA is regulated by the inhibitory effect of testosterone and the stimulatory effect of estrogen in both normal and diabetic mice.

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Section: Discussionmentioning

confidence: 99%

Involvement of gonadal steroid hormone disturbance in altered prolactin receptor gene expression in the liver of diabetic mice

Murakami¹,

Maeda²,

Oka³

1999

Journal of Endocrinology

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“…Coleman & Burkart (1977) have reported that plasma corticosterone levels are elevated in diabetes mice, whilst Carson, Hanker & Kirschner (1982) reported an increase in adrenal catecholamines and enzymes involved in their synthesis. Plasma prolactin, growth hormone and insulin at different times in the life span of the mutants have been reported by Sinha, Baxter, Larson & Vanderlaan (1979). Apparently db/db mice show a decreased thyroidal response to thyrotropin (Bagchi, Brown, Shivers, Lucas & Mack, 1981).…”

Section: Miscellaneous Endocrine-relatedfunctionsmentioning

confidence: 99%

Mouse Mutants as Models in Endocrine Research

Charlton

1984

Exp Physiol

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Although Shire (1979) has listed some forty‐eight mouse mutants of interest to the endocrinologist, this short review has concentrated upon eleven mutations which have resulted in a significant number of scientific publications over the last 4 or 5 years. The selection of references has had to be limited, but it should be possible easily to expand the list given in this review. Although the proximate cause of none of the eleven mutations has been identified with certainty, the abnormalities of function have included hormone deficiencies and receptor and post‐receptor malfunctions. It is perhaps a reflexion on our society in the 1980s, that the bulk of research has concentrated on the obese mouse. However, we still do not know the initial cause of this syndrome. The major disadvantage of the mouse to the hormone assayist lies in the small blood volume and the extreme difficulty in taking serial blood samples over a short period of time. With increased sophistication of assay techniques this may prove less daunting, but is an area where a review of the literature reveals discrepancies between laboratories, and even between data generated by the same laboratory at different times. With regard to the hormone content of endocrine tissues, the way forward for peptide‐secreting glands may be in the measurement of mRNA levels for particular hormones. Certainly the methods of recombinant‐DNA technology will yield positive information upon the aetiology and expression of some of the syndromes considered above. Organ transplantation is an area in which mutant mice have proved useful, for example gonadal, pituitary and pancreatic tissue transplantation. The grafting of neural tissue in the hpg mouse has added a further dimension to this field of research. The great infrastructure of genetical research in mice has enabled us to breed mutant genes onto different genetic backgrounds. This area of research is one which deserves to expand. The techniues of in vitro fertilization, chimera formation and embryo transfer have been used, in part, in studies on mouse mutants, and should provide technical means for further investigating gene expression. The family of dwarf mutants are ideally suited for research into the expression of genes micro‐injected into the fertilized egg (see Charlton & Cox, 1983). As new hormones are isolated and become available for study these mouse mutants may well be useful in delineating physiological functions for natural and pharmacological products. Again, the dwarf mutants would seem ideally suited for research into the synthesis and action of GRF. Mouse mutants have proved of use to biochemists and embryologists and provide fertile ground for endocrine investigations ranging from molecular genetics to membrane biophysics.

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“…Several studies have shown that GH levels are decreased in the STZ‐induced diabetic rat and diabetic ( db/db ) mouse (24–27). Therefore, alterations in levels of GH in the STZ‐diabetic rat maydirectlyor indirectly regulate KBP expression.…”

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confidence: 99%

Kallikrein‐binding protein is induced by growth hormone in the dwarf rat

et al. 1999

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Rat kallikrein-binding protein (KBP), a member of the serpin family, is a tissue kallikrein inhibitor. It has been shown to be a potential pathogenic factor of diabetic retinopathy and may play a role in animal development and growth. To determine whether reduced KBP expression is involved in retarded animal growth, we examined the in vivo effect of growth hormone (GH) deficiency on the expression of KBP in the Lewis dwarf (dw/dw). We found that serum levels of functionally active KBP were reduced in the dwarf rat (P < 0.05) as determined by complex formation assay between serum KBP and (125)I-labeled rat tissue kallikrein. Enzyme-linked immunosorbent assay showed that KBP levels were significantly reduced in the serum of the dwarf rat compared to the Lewis rat (213.8 ng/ml vs. 413.8 ng/ml, n = 4, P < 0.01). The decreased KBP levels were confirmed by Western blot analysis. Moreover, treatment of the dwarf rat with recombinant human GH for 4 wk resulted in a significant increase in KBP activity (P < 0.01) and serum KBP levels compared with the untreated dwarf rat (549.8 ng/ml, n = 5, vs. 213.8 ng/ml, n = 4, P < 0.02). Northern blot analysis and densitometry showed that liver KBP mRNA levels were reduced by fivefold in the dwarf rat compared to the Lewis rat and the decrease was reversed by the GH treatment. These results indicate that the KBP levels are regulated at the RNA level. Furthermore, in vitro studies using cultured rat hepatocytes showed that GH may have a direct regulatory effect on KBP expression since KBP levels increased in the conditioned media of cells treated with GH. These results demonstrated that KBP is reduced in the genetic dwarf rat and is restored to normal by GH; therefore, KBP is a GH-dependent protein and may be a new target for studying the mechanism of pathological animal growth.

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Levels of Prolactin, Growth Hormone and Insulin in Genetically Diabetic (db/db) Mice

Cited by 17 publications

References 8 publications

Involvement of gonadal steroid hormone disturbance in altered prolactin receptor gene expression in the liver of diabetic mice

Involvement of gonadal steroid hormone disturbance in altered prolactin receptor gene expression in the liver of diabetic mice

Mouse Mutants as Models in Endocrine Research

Kallikrein‐binding protein is induced by growth hormone in the dwarf rat

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