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ABSTRACT
The effect of transferrin on basal and FSH-stimulated aromatase activity of granulosa cells from immature female rats treated with diethylstilboestrol (DES) was examined in vitro by a radiometric method. The basal activity of the enzyme was very low after 3 days of incubation. Treatment with FSH (20 ng/ml) resulted in a 9·6-fold increase in activity, whereas coincubation with increasing doses of transferrin (3–300 μg/ml) produced a dose-dependent inhibition of FSH-stimulated aromatase activity with a projected minimal effective dose of < 2 μg/ml. A time-course study showed that the inhibitory effect of transferrin on aromatase activity has become significant at 48 h of incubation.
The inhibitory action of transferrin on the enzyme complex was further confirmed by showing that the FSH dose–response curve was significantly suppressed by concomitant treatment with 100 μg transferrin/ml with a maximum suppression of 54·1 % at a dose of 30 ng FSH/ml.
The possibility that transferrin may act through a non-specific inhibitory effect seems unlikely, as no changes in cell number and DNA content per well were observed. In fact, protein synthesis was enhanced after treatment with transferrin. Aromatase activity, stimulated by several promoters of cyclic AMP (cAMP), such as prostaglandin E2 (PGE2), forskolin and 8-bromo-cAMP, was significantly suppressed by 100 μg transferrin/ml (36·6, 47·4 and 23·4% inhibition respectively), suggesting that the effect of transferrin on FSH action may involve a site(s) distal to cAMP generation.
These findings indicated that transferrin, present in follicular fluid, may play an important role in the regulation of granulosa cell differentiation.
Journal of Endocrinology (1991) 131, 245–250
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ABSTRACT
Prostatic steroid-binding protein (PSBP) mRNAs transcribed from the three genes C1, C2 and C3 were quantitated in neonatal rat ventral prostate by Northern blot analysis. Transcription was initiated at day 14 for C1 and C2 and day 10 for C3, and reached mature levels by day 21 for C1 and C2 and day 28 for C3. The changes of both cytoplasmic and nuclear prostatic androgen receptors in 10- to 150-day-old rats were investigated by radioligand assay and showed a fivefold transient increase between days 10 and 28. Thus there was a good correlation between the onset of PSBP gene expression and the transient increase in androgen receptors; increases in receptor concentration may be a prerequisite for changes in gene expression.
J. Endocr. (1988) 117, 361–366
Search for other papers by Xiwen Xiong in
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Search for other papers by Cuicui Zhang in
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SIRT6 is a member of sirtuin family of deacetylases involved in diverse processes including genome stability, metabolic homeostasis and anti-inflammation. However, its function in the adipose tissue is not well understood. To examine the metabolic function of SIRT6 in the adipose tissue, we generated two mouse models that are deficient in Sirt6 using the Cre-lox approach. Two commonly used Cre lines that are driven by either the mouse Fabp4 or Adipoq gene promoter were chosen for this study. The Sirt6-knockout mice generated by the Fabp4-Cre line (Sirt6 f/f :Fabp4-Cre) had a significant increase in both body weight and fat mass and exhibited glucose intolerance and insulin resistance as compared with the control wild-type mice. At the molecular levels, the Sirt6 f/f :Fabp4-Cre-knockout mice had increased expression of inflammatory genes including F4/80, TNFα, IL-6 and MCP-1 in both white and brown adipose tissues. Moreover, the knockout mice showed decreased expression of the adiponectin gene in the white adipose tissue and UCP1 in the brown adipose tissue, respectively. In contrast, the Sirt6 knockout mice generated by the Adipoq-Cre line (Sirt6 f/f :Adipoq-Cre) only had modest insulin resistance. In conclusion, our data suggest that the function of SIRT6 in the Fabp4-Cre-expressing cells in addition to mature adipocytes plays a critical role in body weight maintenance and metabolic homeostasis.
Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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The level of the obese gene product leptin is often positively correlated with body weight, supporting the notion that hyperleptinemia contributes to obesity-associated cardiac dysfunction. However, a link between leptin levels and cardiac function has not been elucidated. This study was designed to examine the role of leptin deficiency (resulting from a point mutation of the leptin gene) in cardiomyocyte contractile function. Mechanical properties and intracellular Ca2 + transients were evaluated in ventricular myocytes from lean control and leptin-deficient ob/ob obese mice at 12 weeks of age. Cardiac ultrastructure was evaluated using transmission electron microscopy. ob/ob mice were overtly obese, hyperinsulinemic, hypertriglycemic, hypoleptinemic and euglycemic. Ultrastructural examination revealed swelling and disorganization of cristae in mitochondria from ob/ob mouse ventricular tissues. Cardiomyocytes from ob/ob mice displayed reduced expression of the leptin receptor Ob-R, larger cross-sectional area, decreased peak shortening and maximal velocity of shortening/relengthening, and prolonged relengthening but not shortening duration compared with lean counterparts. Consistent with mechanical characteristics, myocytes from ob/ob mice displayed reduced intracellular Ca2 + release upon electrical stimulus associated with a slowed intracellular Ca2 + decay rate. Interestingly, the contractile aberrations seen in ob/ob myocytes were significantly improved by in vitro leptin incubation. Contractile dysfunction was not seen in age- and gender-matched high fat-induced obese mice. These results suggested that leptin deficiency contributes to cardiac contractile dysfunction characterized by both systolic and diastolic dysfunction, impaired intracellular Ca2 + hemostasis and ultrastructural derangement in ventricular myocytes.
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Search for other papers by Yang Zhang in
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Department of Endocrinology and Metabolism, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China
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Search for other papers by X Charlie Dong in
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Chronic exposure of pancreatic β-cells to abnormally elevated levels of free fatty acids can lead to β-cell dysfunction and even apoptosis, contributing to type 2 diabetes pathogenesis. In pancreatic β-cells, sirtuin 6 (SIRT6) has been shown to regulate insulin secretion in response to glucose stimulation. However, the roles played by SIRT6 in β-cells in response to lipotoxicity remain poorly understood. Our data indicated that SIRT6 protein and mRNA levels were reduced in islets from diabetic and aged mice. High concentrations of palmitate (PA) also led to a decrease in SIRT6 expression in MIN6 β-cells and resulted in cell dysfunction and apoptosis. Knockdown of Sirt6 caused an increase in cell apoptosis and impairment in insulin secretion in response to glucose in MIN6 cells even in the absence of PA exposure. Furthermore, overexpression of SIRT6 alleviated the palmitate-induced lipotoxicity with improved cell viability and increased glucose-stimulated insulin secretion. In summary, our data suggest that SIRT6 can protect against palmitate-induced β-cell dysfunction and apoptosis.
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Clinical and animal studies have shown that treatment with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II (Ang II) receptor antagonists slows the progression of nephropathy in diabetes, indicating that Ang II plays an important role in its development. We have reported previously that insulin inhibits the stimulatory effect of high glucose levels on angiotensinogen (ANG) gene expression in rat immortalized renal proximal tubular cells (IRPTCs) via the mitogen-activated protein kinase (p44/42 MAPK) signal transduction pathway. We hypothesize that the suppressive action of insulin on ANG gene expression might be attenuated in renal proximal tubular cells (RPTCs) of rats with established diabetes. Two groups of male adult Wistar rats were studied: controls and streptozotocin (STZ)-induced diabetic rats at 2, 4, 8 and 12 weeks post-STZ administration. Kidney proximal tubules were isolated and cultured in either normal glucose (i.e. 5 mM) or high glucose (i.e. 25 mM) medium to determine the inhibitory effect of insulin on ANG gene expression. Immunoreactive rat ANG (IR-rANG) in culture media and cellular ANG mRNA were measured by a specific radioimmunoassay and reverse transcription-polymerase chain reaction assay respectively. Activation of the p44/42 MAPK signal transduction pathway in rat RPTCs was evaluated by p44/42 MAPK phosphorylation employing a PhosphoPlus p44/42 MAPK antibody kit. Insulin (10(-7) M) inhibited the stimulatory effect of high glucose levels on IR-rANG secretion and ANG gene expression and increased p44/42 MAPK phosphorylation in normal rat RPTCs. In contrast, it failed to affect these parameters in diabetic rat RPTCs. In conclusion, our studies demonstrate that hyperglycaemia induces insulin resistance on ANG gene expression in diabetic rat RPTCs by altering the MAPK signal transduction pathway.
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We recently found that the oxytocin receptor (OTR) is expressed in the human and rabbit corpus cavernosum and mediates contractility in vitro. The present study extended our investigations to the rat, and explored whether OTR regulates penile detumescence in vivo. Real-time RT-PCR quantitatively characterized the distribution of OTR mRNA in the male genital tract. Specific transcripts for OTR were expressed in all the tissues investigated. Penile expression of OTR was comparable to that observed in testis and prostate. Western blot analysis detected a single band of the expected molecular mass for OTR in all tissues examined, including rat penis. Expression of OTR protein in rat penile extracts was further confirmed by binding studies, using the OTR selective radiolabeled ligand 125I-OTA (K d=17 ± 6.5 pM, Bmax=15.7 ± 5 fmoles/mg protein). OTR was immunolocalized to the endothelial and smooth muscle compartments of cavernous spaces and blood vessels. In rat corpus cavernosum strips, oxytocin (OT) and an OTR selective agonist ([Thr4,Gly7]OT) induced identical increases in tension, while different vasopressin agonists were less active. In vivo, OT intra-cavernous injection (ICI) dose-dependently inhibited intracavernous pressure (ICP) increase elicited by either electrical stimulation of the cavernous nerve or ICI of papaverine with similar IC50s (117.7 ± 37 mU). The OTR antagonist, atosiban, counteracted the contractile effect of OT both in vitro and in vivo. Atosiban alone significantly increased ICP at lower stimulation frequencies (2 Hz=P<0.001 and 4 Hz=P<0.05 vs control), but not at the maximal frequency (16 Hz). Our data showed that OTR is present in the rat penis and mediates contractility both in vitro and in vivo, therefore suggesting a role for OT in maintaining penile detumescence.
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Pancreatic β cells adapt to pregnancy-induced insulin resistance by unclear mechanisms. This study sought to identify genes involved in β cell adaptation during pregnancy. To examine changes in global RNA expression during pregnancy, murine islets were isolated at a time point of increased β cell proliferation (E13.5), and RNA levels were determined by two different assays (global gene expression array and G-protein-coupled receptor (GPCR) array). Follow-up studies confirmed the findings for select genes. Differential expression of 110 genes was identified and follow-up studies confirmed the changes in select genes at both the RNA and protein level. Surfactant protein D (SP-D) mRNA and protein levels exhibited large increases, which were confirmed in murine islets. Cytokine-induced expression of SP-D in islets was also demonstrated, suggesting a possible role as an anti-inflammatory molecule. Complementing these studies, an expression array was performed to define pregnancy-induced changes in expression of GPCRs that are known to impact islet cell function and proliferation. This assay, the results of which were confirmed using real-time reverse transcription-PCR assays, demonstrated that free fatty acid receptor 2 and cholecystokinin receptor A mRNA levels were increased at E13.5. This study has identified multiple novel targets that may be important for the adaptation of islets to pregnancy.
Department of Medicine-Gastroenterology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
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Department of Medicine-Gastroenterology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
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Department of Medicine-Gastroenterology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
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Department of Medicine-Gastroenterology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
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Department of Medicine-Gastroenterology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
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Department of Medicine-Gastroenterology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
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Department of Medicine-Gastroenterology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
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Department of Medicine-Gastroenterology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
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The cystic fibrosis transmembrane conductance regulator (CFTR) is one of the most intensively investigated Cl− channels. Different mutations in the CFTR gene cause the disease cystic fibrosis (CF). CFTR is expressed in the apical membrane of various epithelial cells including the intestine. The major organ affected in CF patients is the lung, but it also causes an important dysfunction of intestinal ion transport. The modulation of CFTR mRNA expression by atrial natriuretic peptide (ANP) was investigated in rat proximal colon and in human intestinal CaCo-2 cells by RNase protection assay and semi-quantitative reverse transcriptase PCR techniques. Groups of rats subjected to volume expansion or intravenous infusion of synthetic ANP showed respective increases of 60 and 50% of CFTR mRNA expression in proximal colon. CFTR mRNA was also increased in cells treated with ANP, reaching a maximum effect at 10−9 M ANP, probably via cGMP. ANP at 10−9 M was also able to stimulate both the CFTR promoter region (by luciferase assay) and protein expression in CaCo-2 cells (by Western blot and immunoprecipitation/phosphorylation). These results suggested the involvement of ANP, a hormone involved with extracellular volume, in the expression of CFTR in rat proximal colon and CaCo-2 intestinal cells.
