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The metabolism of testosterone was studied in vitro in anterior pituitary, hypothalamic and hyperstriatal tissues taken from male European starlings in the autumn. In all the tissues studied, testosterone was converted into 5α-androstan-17β-ol-3-one (5α-DHT), 5β-androstan-17β-ol-3-one (5β-DHT), 5β-androstane-3α,17β-diol (5β-THT), 5β-androstane-3,-17-dione and androst-4-ene-3,17-dione.
The 5α-DHT was produced in significantly greater amounts by the pituitary gland than by the hypothalamus and hyperstriatum. The amount of 5α-DHT produced, however, was very low in comparison with the amounts of 5β-reduced metabolites. The amount of 5β-reductase was also higher in the pituitary gland than in the two nervous tissues. The ratios between the production of 5β-DHT, 5β-THT and 5β-androstane-3,17-dione were, however, different in the three tissues: 5β-DHT was produced in the greatest quantities by the hyperstriatum, while the production of 5β-THT, 5β-androstane-3,17-dione and androst-4-ene-3,17-dione was greatest in pituitary tissue.
The role of 5α- and 5β-reduced metabolites in the pituitary gland and in the brain of birds is unknown, but some possibilities arising from the present results are discussed.
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Testosterone metabolism was studied in vitro in the prostate of intact and castrated golden hamsters maintained either in short days (8 h light: 16 h darkness, 8L : 16D) or in long days (14L : 10D). Testosterone was found to be converted into 17β-hydroxy-5α-androstan-3-one (5α-DHT), 5α-androstane-3α, 17β-diol, 5α-androstane-3, 17-dione and androstenedione. The mean conversion of testosterone to 5α-DHT was higher in prostates from animals maintained in long days than in short days (P < 0·0025) while that to androstenedione was higher in short days (P <0·0005); no significant changes in the formation of the other three metabolites were noted. Castration of animals maintained in short days resulted in a significant (P <0·05) decrease in the mean conversion to all four metabolites. In contrast, castration of animals kept in a long-day regime caused a significant (P <0·01) decrease in the mean formation of 5α-DHT but a significant (P <0·05) increase in the mean formation of 5α-androstane-3α, 17β-diol.
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A cloacal gland complex whose growth and development is androgen-dependent exists in the Japanese quail. In-vitro incubation studies of the cloacal gland using 4-14C-labelled testosterone as substrate allowed the positive identification of five metabolites: androstenedione, 5β-dihydrotestosterone (5β-DHT), 5β-androstane-3α,17β-diol, 5α-DHT and 5α-androstane-3α,17β-diol. More polar metabolites, not yet chemically identified, were detected in trace amounts. Androstenedione appeared to be the main testosterone metabolite in immature birds while in mature birds on long daylengths testosterone was preferentially metabolized to 5α-DHT. This change may have been in response to the higher levels of plasma steroids found in mature birds. When various testosterone metabolites, contained in silicone elastomer capsules, were implanted s.c. into castrated birds maintained on a photostimulatory light régime, 5α-DHT, 5α-androstane-3,17-dione, androstenedione and 5α-androstan-3α-ol-17-one were shown to be equipotent with testosterone in stimulating the development of the cloacal gland. 5α-Androstane-3α,17β-diol and 5α-androstan-3β-ol-17-one stimulated some growth while 5β-DHT, 5α-androstane-3β,17β-diol, 5α-androstane-3α,17β-diol, 5β-androstane-3,17-dione, androst-5-en-3β-ol-17-one and androst-5-ene-3β,17β-diol were completely ineffective.
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Department of Endocrinology, University of Milan, Via A. del Sarto 21, 20129 Milan, Italy
(Received 8 May 1978)
It is well established that the rat prostate gland converts testosterone mainly into 5α-androstan-17β-ol-3-one (5α-dihydrotestosterone, 5α-DHT) and to a lesser extent into 5α-androstan-3α,17β-diol (5α-tetrahydrotestosterone, 5α-THT). This occurs, both in vivo and in vitro, through the action of a 5α-reductase and a 3α-hydroxysteroid dehydrogenase system (Baulieu, Lasnitzki & Robel, 1968; Bruchovsky & Wilson, 1968; Gloyna & Wilson, 1969; Kniewald, Massa & Martini, 1971). It has also been recognized that, although the 5α-reduction of testosterone is an irreversible reaction, the reduction of 5α-DHT to 5α-THT is reversible (Becker, Grabosch, Hoffmann & Voigt, 1973; Cresti & Massa, 1977). Consequently, the question has been raised as to whether the biological actions of 5α-THT are attributable to the compound as such or to 5α-DHT. At the anterior pituitary level, 5α-reductase activity is increased by castration and decreased
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The aim of this work was to study the possible relationship between pancreatic duodenal homeobox-1 (Pdx-1) and islet neogenesis-associated protein (INGAP) during induced islet neogenesis. Pregnant hamsters were fed with (S) and without (C) sucrose, and glycemia, insulin secretion in vitro, and pancreas immunomorphometric parameters were measured in their 7-day-old offspring. S offspring had significantly lower glycemic levels than C animals. Insulin release in response to increasing glucose concentrations in the incubation medium (2-16 mM glucose) did not increase in pancreata from either C or S offspring. However, pancreata from S offspring released more insulin than those from C animals. In S offspring, beta-cell mass, beta-cell replication rate and islet neogenesis increased significantly, with a simultaneous decrease in beta-cell apoptotic rate. INGAP- and Pdx-1-positive cell mass also increased in the islets and among acinar and duct cells. We found two subpopulations of Pdx-1 cells: INGAP-positive and INGAP-negative. Pdx-1/INGAP-positive cells did not stain with insulin, glucagon, somatostatin, pancreatic polypeptide, or neurogenin 3 antibodies. The increment of Pdx-1/INGAP-positive cells represented the major contribution to the Pdx-1 cell mass increase. Such increments varied among pancreas subsectors: ductal>insular>extrainsular. Our results suggested that INGAP participates in the regulation of islet neogenesis, and Pdx-1/INGAP-positive cells represent a new stem cell subpopulation at an early stage of development, highly activateable in neogenesis.
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Administration of a sucrose-rich diet (SRD) to normal hamsters induces an insulin-resistant state and a significant increase of insulin secretion and β-cell mass. Islets isolated from these animals had a marked increase in glucose metabolism and glucose-induced insulin secretion, at both low and high glucose concentrations. They also presented increased hexokinase (HK) activity, without measurable changes in glucokinase (GK) activity. In this study we measured HK and GK activity in homogenates of islets isolated from normal control and SRD-fed hamsters, as well as in their particulate and cytosolic fractions. We also measured transcription rate (mRNA by reverse transcriptase PCR) and expression levels (Western blotting) of both enzymes in these islets. We found an increase in HK activity and expression levels, without measurable changes in HK mRNA level in SRD-fed animals. Whereas a similar GK activity was measured in homogenates of islets isolated from both groups, such activity was significantly higher in the cytosolic fraction of SRD islets. On the other hand, GK transcription rate and expression level were similar in both experimental groups. Our results suggest that the increased β-cell secretory response to low glucose can be partly ascribed to an increased activity of islet HK consecutive to an enhanced expression of the enzyme, while the enhanced response to high glucose could be due to changes in GK compartmentalization.
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The possible relationship between changes in islet cell mass and in islet neogenesis-associated protein (INGAP)-cell mass induced by sucrose administration to normal hamsters was investigated. Normal hamsters were given sucrose (10% in drinking water) for 5 (S8) or 21 (S24) weeks and compared with control (C) fed hamsters. Serum glucose and insulin levels were measured and quantitative immunocytochemistry of the endocrine pancreas was performed. Serum glucose levels were comparable among the groups, while insulin levels were higher in S hamsters. There was a significant increase in beta-cell mass (P<0.02) and in beta-cell 5-bromo-2'-deoxyuridine index (P<0.01), and a significant decrease in islet volume (P<0.01) only in S8 vs C8 hamsters. Cytokeratin (CK)-labelled cells were detected only in S8 hamsters. INGAP-positive cell mass was significantly larger only in S8 vs C8 hamsters. Endocrine INGAP-positive cells were located at the islet periphery ( approximately 96%), spread within the exocrine pancreas ( approximately 3%), and in ductal cells (<1%) in all groups. INGAP positivity and glucagon co-localization varied according to topographic location and type of treatment. In C8 hamsters, 49.1+/-6. 9% cells were INGAP- and glucagon-positive in the islets, while this percentage decreased by almost half in endocrine extra-insular and ductal cells. In S8 animals, co-expression increased in endocrine extra-insular cells to 36.3+/-9.5%, with similar figures in the islets, decreasing to 19.7+/-6.9% in ductal cells. INGAP-positive cells located at the islet periphery also co-expressed CK. In conclusion, a significant increase of INGAP-positive cell mass was only observed at 8 weeks when neogenesis was present, suggesting that this peptide might participate in the control of islet neogenesis. Thus, INGAP could be a potentially useful tool to treat conditions in which there is a decrease in beta-cell mass.
Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System and University of Washington, Seattle, Washington 98108, USA
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Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System and University of Washington, Seattle, Washington 98108, USA
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Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System and University of Washington, Seattle, Washington 98108, USA
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Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System and University of Washington, Seattle, Washington 98108, USA
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Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System and University of Washington, Seattle, Washington 98108, USA
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Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System and University of Washington, Seattle, Washington 98108, USA
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Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System and University of Washington, Seattle, Washington 98108, USA
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Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System and University of Washington, Seattle, Washington 98108, USA
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The increasing production of genetically-modified mouse models has necessitated studies to determine the inherent physiological characteristics of commonly used mouse strains. In this study we examined insulin secretory function in response to an intravenous bolus of glucose or glucose plus arginine in anesthetized C57BL/6, DBA/2 and 129T2 mice fed either a control or high fat diet for 6 weeks. The results show that 129T2 mice had higher fasting plasma glucose levels and lower fasting plasma insulin levels compared with C57BL/6 and DBA/2 mice regardless of diet. Furthermore, 129T2 mice were glucose intolerant and secreted significantly less insulin in response to glucose and glucose plus arginine irrespective of diet compared with the other two strains of mice. DBA/2 mice hypersecreted insulin in response to glucose and glucose plus arginine compared with C57BL/6 and 129T2 mice. Moreover while first phase insulin secretion was appropriately increased in response to the high fat diet in C57BL/6 and 129T2 mice, this was not the case for DBA/2 mice. Mean islet area was decreased in response to a high fat diet in DBA/2 mice, while there was no dietary effect on the other two strains. This study highlights the inherent genetic differences that exist among seemingly normal strains of mice that are commonly used to make transgenic and knockout mice. Understanding these differences will provide researchers with the information to choose the appropriate genetic background on which to express their particular genetic alteration.
