Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to assess human intracranial tumours for their gene expression pattern of the vasoactive peptide adrenomedullin (AM), its receptor (AM-R) and leptin, which exerts multiple biological effects including proliferation and angiogenesis via the leptin receptor (OB-Rb). Gene activity of neuropeptide Y (NPY) was monitored additionally. We investigated whether there was a characteristic gene expression pattern of AM and leptin in different intracranial tumours, depending on their proliferation activity and biological behaviour. We investigated 35 non-functioning pituitary adenomas (including eight null cell, four silent plurihormonal, 23 silent gonadotroph adenomas), seven somatotropinomas, seven prolactinomas, eight meningiomas, five astrocytomas, two glioblastoma multiformes and unaffected temporal lobe (n = 8). Quantitative reverse transcriptase-polymerase chain reaction (TaqMan RT-PCR) was performed. AM mRNA was detectable in all tumour specimens. AM/GAPDH (glyceraldehyde-3-phosphate dehydrogenase) ratio was significantly higher in somatotropinomas, as was AM/CD31 ratio in prolactinomas, compared with inactive adenomas (P < 0.05). AM-R mRNA was found in all tumour subgroups in small quantities but, in general, higher in tumours than in temporal lobe tissue, respectively. AM-R/CD31 ratio was significantly higher in prolactinomas than in inactive adenomas (P < 0.05). Leptin was detectable in very low quantities in each subgroup. OB-Rb gene expression was found in all tumour subgroups, OB-Rb/GAPDH ratio was highest for meningiomas (P < 0.0001, compared with temporal lobe). NPY mRNA was detectable in temporal lobe in higher quantities than in tumours (P < 0.0001), and almost undetectable in prolactinomas and astrocytomas. Our data demonstrate that AM and AM-R, NPY, as well as leptin and OB-Rb, are expressed in various intracranial tumours in humans but their particular function has to be elucidated further. At present, there is no evidence for a cross-talk on transcriptional level between the peptidergic vasodilative system AM and the putative angiogenic and proliferation affecting factor leptin.
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PMID:Gene expression of adrenomedullin, leptin, their receptors and neuropeptide Y in hormone-secreting and non-functioning pituitary adenomas, meningiomas and malignant intracranial tumours in humans. 1148 41

The adipose hormone leptin and its receptor are important for regulation of food intake and energy metabolism. Leptin also is involved in the growth of different tissues. In this study, we show the expression of leptin in primary cultures of normal human osteoblasts (hOBs) as evidenced by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunocytochemistry. Release of leptin into the medium also was found. Leptin was not detected in commercially available hOBs (NHOst) or in three different human monoclonal osteosarcoma cell lines. Leptin expression was observed in OBs in the mineralization and/or the osteocyte transition period but not during the matrix maturation period. Furthermore, hOBs and osteosarcoma cell lines expressed the long signal-transducing form of the leptin receptor (OB-Rb) as shown by RT-PCR. We observed no significant changes in leptin or OB-Rb genes in hOBs after incubation with recombinant leptin, indicating no autoregulation of the leptin expression. Incubation of both hOBs entering the mineralization phase and osteosarcoma cell lines with recombinant leptin markedly increased the number of mineralized nodules as shown by alizarin S staining. These findings indicate that leptin may be of importance for osteoblastic cell growth and bone mineralization.
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PMID:Leptin is expressed in and secreted from primary cultures of human osteoblasts and promotes bone mineralization. 1205 70

Leptin receptor (leptin-R) is a polypeptide consisting of a single transmembrane-spanning component. Recent studies performed by reverse transcriptase polymerase chain reaction (RT-PCR) have shown the production of leptin-R in various tissues including the pituitary, hypothalamus and reproductive organs. The localization of leptin-R protein in the pituitary gland, however, has not been extensively studied. This study deals with the expression of leptin-R in the normal rat pituitary gland, which was disclosed primarily in the plasma membrane fraction by immunoblotting and immunohistochemical staining methods. Double immunohistochemical staining revealed that the colocalization of leptin-R and anterior pituitary hormone expression was seen mainly in growth hormone (GH)-secreting cells (97.4 +/- 1.3%; GH-positive cells/leptin-R-positive cells), but in less than 1% of prolactin (PRL)-, adrenocorticotropic hormone (ACTH)-, thyroid-stimulating hormone-beta (TSH beta)- and follicle-stimulating hormone-beta (FSH beta)/luteinizing hormone-beta (LH beta)-positive cells. In contrast, leptin was localized most frequently in FSH beta/LH beta- and less frequently in TSH beta-positive cells. The above findings suggest that, in the rat anterior pituitary gland, there are paracrine relationships between leptin-producing cells and cells with leptin-R, which may regulate the function of GH cells.
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PMID:Expression and localization of leptin receptor in the normal rat pituitary gland. 1157 88

There is evidence for interactions between leptin and cholecystokinin in controlling food intake. Since cholecystokinin acts on vagal afferent neurones, we asked whether the leptin receptor was also expressed by these neurones. Primers for different forms of the leptin receptor were used in reverse transcriptase-polymerase chain reaction (RT-PCR) of rat and human nodose ganglia. RT-PCR yielded products corresponding to the long (functional) form as well as short forms of the rat leptin receptor. Moreover, RT-PCR revealed the long form of the leptin receptor in a human nodose ganglion. The identities of RT-PCR products were confirmed by sequencing. Primers corresponding to leptin itself did not give RT-PCR products in nodose ganglia. Immunocytochemical studies revealed leptin-receptor immunoreactivity in neuronal cell bodies. Many neurones co-expressed the leptin and cholecystokinin type A receptors, or leptin receptor and cocaine- and amphetamine-related transcript. We conclude that vagal afferent neurones that express the cholecystokinin type A receptor and cocaine- and amphetamine-related transcript, may also express the long form of the leptin receptor providing a neurochemical basis for observations of interactions between cholecystokinin and leptin.
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PMID:Expression of the leptin receptor in rat and human nodose ganglion neurones. 1180 69

It has been reported recently that the stomach can produce and store leptin and release it, both into the blood and into the gastrointestinal lumen, in response to food intake. Here, we have followed the ontogenic pattern of leptin mRNA expression and leptin levels in stomach during the perinatal period, which were compared with adults. Leptin mRNA expression was assessed by reverse transcriptase-polymerase chain reaction, and tissue leptin content by enzyme-linked immunosorbent assay and localised by immunohistochemistry. Leptin mRNA is expressed at low levels in rat stomach in prenatal stages. It increased from 4 to 8 hr of life in suckling rats, an increase not observed in the fasted pups, which were separated from their mothers immediately after birth. Leptin expression rose steadily after birth during the first month of life, with a marked increase from 15-day-old rats, followed by a parallel increase in leptin levels from day 21 of life, which was coincident with the change from suckling to a solid diet. The immunohistochemical analysis showed leptin immunoreactivity at different levels of the stomach mucosa, suggesting that during early development leptin could derive from different sources. During the pre- and neonatal periods, leptin is mainly located at the superficial epithelium (suggesting maternal origin from amniotic cells and mammary glandular cells, respectively). At the beginning of the chow diet, the stomach produces leptin in the glands (main source from 15 days of life), suggesting an endogenous production of the protein after that period. The present work demonstrates the expression of leptin mRNA and leptin protein in the stomach of neonate rats, and shows that the ontogenic profile of leptin appearance in the stomach during the perinatal period is probably related to the onset of suckling and to the change of diet from milk to solid chow.
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PMID:Perinatal expression of leptin in rat stomach. 1180 78

We have previously shown that maternal intake of essential fatty acids during late gestation and lactation affects the level of serum leptin in pups. The aim of the present study was to investigate the effect of dietary essential fatty acids on leptin content in the milk of rat dams and leptin expression in white adipose tissue of pups during the suckling period. During late gestation and throughout lactation, rats were fed a control or an essential fatty acid-deficient (EFAD) diet. Milk of the EFAD dams contained more saturated and less polyunsaturated fatty acids compared with the control dams. Milk leptin levels were higher in the EFAD dams than in the control dams at 3 wk of lactation. The weight of inguinal white adipose tissue depots and the serum leptin levels of the EFAD pups were significantly lower than in the control pups during the whole suckling period. In addition, semiquantitative reverse transcriptase-PCR analysis of leptin mRNA levels in inguinal white adipose tissue showed a reduction in the EFAD pups compared with the control pups at 3 wk of age. We conclude that maternal dietary essential fatty acid intake affects serum leptin levels in pups by regulating both the amount of adipose tissue and the leptin mRNA expression.
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PMID:Maternal dietary intake of essential fatty acids affects adipose tissue growth and leptin mRNA expression in suckling rat pups. 1208 51

Recently, leptin has been shown to play a regulatory role for differentiation within the myeloid and erythroid cell lineage, whereas results of its regulatory effects on lymphocytes and related tumor cells have been contradictory. To investigate whether leptin plays a role in acute lymphoblastic leukemia (ALL), we investigated the levels of leptin in plasma with enzyme-linked immunosorbent assays and the expression of the leptin receptor on malignant lymphoblasts with reverse transcriptase polymerase chain reaction (RT-PCR). At diagnosis, the leptin levels of bone marrow-derived plasma in children with ALL were found to be significantly lower than the levels of healthy control subjects (0.92 +/- 0.79 ng/mL versus 3.01 +/- 2.27 ng/mL, respectively). Notably, at complete hematologic remission (at day 33 of chemotherapy), leptin levels had normalized to 2.6 +/- 2.4 ng/mL. To elucidate the underlying mechanism of this phenomenon, we analyzed the expression of the leptin receptor on the mononuclear cell populations of the patients. RT-PCR analysis revealed gene expression rates of 33% at diagnosis versus 71% at remission, compared with 100% for healthy control subjects. Results of immunohistochemical staining supported these findings by showing that the tumor clones themselves do not express the leptin receptor. Finally, some hypotheses that might explain the decrease of leptin levels in the presence of the tumor clone are discussed.
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PMID:Plasma leptin and leptin receptor expression in childhood acute lymphoblastic leukemia. 1251 39

A lipodystrophic syndrome and metabolic abnormalities have been observed in HIV-infected patients treated with highly active antiretroviral therapy (HAART). A murine model of lipodystrophy is associated with decreased levels of adiponectin, an adipocyte-secreted protein, the administration of which improves the metabolic syndrome in these mice. To investigate the association of adiponectin with metabolic changes in human lipodystrophy, we conducted a cross-sectional study of 112 HIV-infected patients treated with HAART. Mean adiponectin levels were higher in patients with no fat redistribution (FR) vs. FR (4.8 +/- 5.0 vs. 2.2 +/- 2.7 microg/ml, P < 0.01), but no significant differences in adiponectin levels were observed between FR subgroups. The difference in adiponectin levels between subjects with and without FR remained significant after adjusting for age, gender, leptin, HIV medication use, and CD4 count using logistic regression (odds ratio, 0.54, P = 0.008). Adiponectin was significantly correlated with triglycerides (r = -0.40), abdominal visceral fat (r = -0.35), extremity fat (r = 0.37), insulin resistance (HOMA-IR) (r = -0.28), nucleoside reverse transcriptase inhibitor (NRTI) use (r = -0.32), and high-density lipoprotein (HDL) (r = 0.41) using bivariate analysis (all P < 0.01). The association with HDL weakened but remained significant on multivariate analysis (standard beta = 0.29, P = 0.01). However, the association of adiponectin with HOMA-IR became nonsignificant after adjusting for NRTI use (standard beta = -0.15, P = 0.12), suggesting that changes in adiponectin levels may underlie the effect of NRTI use on insulin resistance. The associations of adiponectin with triglycerides and HOMA-IR were also slightly weakened after adjusting for visceral and extremity fat, indicating that adiponectin may, in part, mediate the effect of FR on triglycerides and insulin resistance. This study indicates that adiponectin is inversely correlated with abdominal visceral fat mass, serum triglycerides, and insulin resistance and is directly correlated with HDL and extremity fat in a sample of HIV-infected patients treated with HAART. The results also indicate that NRTI use may worsen insulin resistance by decreasing adiponectin levels. Thus, adiponectin replacement may be a potential treatment option to ameliorate the metabolic changes observed in this patient population.
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PMID:Hypoadiponectinemia is associated with insulin resistance, hypertriglyceridemia, and fat redistribution in human immunodeficiency virus-infected patients treated with highly active antiretroviral therapy. 1257 92

During fetal life, placental tissue represents an additional source of leptin for the mother and conceptus. It has been suggested that feto-placental production of leptin may be involved in placental and fetal growth regulation. The aim of this study was to examine the correlation between leptin mRNA expression in the placenta and the concentrations of leptin in cord blood. A total of 30 healthy, pregnant women who gave birth to healthy neonates were included in the study. Maternal blood (obtained from the cubital vein) and umbilical cord blood were drawn immediately after birth. Serum leptin concentration was determined by enzyme-linked immunosorbent assay and serum insulin concentration was measured by radioimmunoassay. Leptin mRNA was measured in placental tissue by a reverse transcriptase-polymerase chain reaction. The estimated mean leptin mRNA expression in placenta was 4.65 +/- 1.83 pg mRNA/microg DNA. Leptin mRNA correlated with cord serum leptin concentrations (r = 0.3691, p = 0.045). Placental weight correlated with placental leptin mRNA (r = 0.3686, p = 0.045). The mean leptin concentration in cord serum at birth was slightly lower (3.1 +/- 1.9 ng/ml) than that found in maternal serum (3.9 +/- 1.2 ng/ml). A positive correlation was observed between cord and maternal serum leptin levels (r = 0.58, p = 0.001). The mean insulin concentration in maternal serum was not significantly higher than that in umbilical serum: 22.2 +/- 17.8 microIU/ml vs. 6.9 +/- 3.6 microIU/ml; r = 0.069, p = 0.71). Neither maternal nor umbilical insulin concentrations correlated with leptin concentration in cord or maternal peripheral serum.
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PMID:Leptin messenger ribonucleic acid (mRNA) content in the human placenta at term: relationship to levels of leptin in cord blood and placental weight. 1450 75

The recent clinical use of potent HIV-1 drugs, including nucleoside reverse transcriptase inhibitors (NRTIs) and non-peptidic viral protease inhibitors (PIs), and their combinations, termed highly active antiretroviral therapy (HAART), has dramatically reduced the infection-related mortality of AIDS patients, but it is associated with severe metabolic adverse events such as lipodystrophy syndrome, dyslipidaemia, insulin resistance and diabetes mellitus. The aetiology of this syndrome and metabolic alterations appear to be multifactorial, including HIV drug inhibitory effects on adipocyte differentiation, alteration of mitochondrial functions in adipocytes and altered leptin, adiponectin and cytokine expression in adipose tissue of patients. Adipose tissue may thus be a central regulator in disorganized lipid metabolism and insulin resistance associated with antiretroviral therapy, and we propose in this review to explore how adipose tissue may be a target, but also an actor, in the aetiopathogenesis of the lipodystrophy syndrome.
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PMID:Adipocytes targets and actors in the pathogenesis of HIV-associated lipodystrophy and metabolic alterations. 1513 78


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