Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P50502 (Hip)
 7,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Plasma dipeptidyl carboxypeptidase-1 (DCP1; angiotensin I-converting enzyme, kininase II; EC 3.4.15.1) tracks with the deletion allele in genotypes of a 287 bp insertion/deletion (I/D) polymorphism of its gene, DCP1, in healthy Caucasian populations. The aim of the present study was to see whether genotype has a similar influence on plasma DCP1 in hypertensives. 2. The study involved 35 Caucasian patients with severe, familial essential hypertension, who were not being treated with DCP1 inhibitors, and 94 normotensives. Genotyping for the I/D polymorphism was performed by polymerase chain reaction and plasma DCP1 activity was measured by rate of hydrolysis of both [3H]-Hip-Gly-Gly and Hip-His-Leu. 3. Plasma DCP1 activity (nmol Gly-Gly/min per mL; mean +/- s.e.m.) was 67 +/- 2, 82 +/- 4 and 91 +/- 6 in II, ID and DD hypertensives, respectively, which was similar to values of 68 +/- 4, 82 +/- 3 and 94 +/- 3 in normotensives (P = 0.0001 by one-way analysis of variance). Results for the His-Leu assay indicated similar tracking with genotype. 4. The Michaelis constant (mumol Hip-Gly-Gly/mL; mean +/- s.e.m., n = 10) for DD subjects was the same as for II subjects (10.6 +/- 1.6 vs 11.1 +/- 2.3; P = 0.86). 5. In conclusion, in severely hypertensive Caucasian subjects, plasma DCP1 activity is subject to a similar genotypic influence in hypertensives as has been reported previously in normotensives. Furthermore, the plasma DCP1 enzyme itself appears to be functionally similar for each genotype.
 ...
PMID:Genotypic influence on plasma dipeptidyl carboxypeptidase-1 activity in hypertensives. 792 4

The aim of the study was to elucidate the role of hyperinsulinaemia/insulin resistance in hypertension of lean postmenopausal women. Twenty-four women with essential hypertension (systolic/diastolic > or =140/90 mm Hg) and a body mass index (BMI) less than 26 kg/m(2) not receiving antihypertensive treatment or who had been without treatment for a 4-week washout period, and 10 normotensive postmenopausal weight- and aged-matched controls were compared. Both groups were not receiving hormone replacement therapy. Hip and waist circumferences were measured and waist/hip ratios were calculated. Casual blood pressure was measured in triplicate. Neither the fasting plasma glucose nor serum insulin levels in hypertensive women and normotensives differed significantly. During 2 h oral glucose (75 g)-tolerance test the mean plasma glucose levels after 30 min (172.5 +/- 40.24 mg/dl vs. 143.67 +/- 20.16 mg/dl), 60 min (134.88 +/- 38.78 mg/dl vs. 112.33 +/- 5.44 mg/dl) and 120 min (116.08 +/- 26.65 mg/dl vs. 95.56 +/- 20.17 mg/dl) were significantly higher in hypertensives than that for normotensives (P < 0.05 for all three comparisons). The mean serum insulin levels of hypertensive women were significantly higher than that in normotensives after 15 min (92.04 +/- 59.90 microU/ml vs. 54.89 +/- 33.67 microU/ml) and 120 min (49.63 +/- 44.45 microU/ml vs. 19.22 +/- 24.10 microU/ml; P< 0.05 for both comparisons). The mean serum insulin: plasma glucose ratio for hypertensive women was significantly higher than that for normotensives after 15 min (0.596 +/- 0.46 vs. 0.359 +/- 0.20 microU/mg), 60 min (0.406 +/- 0.30 vs. 0.329 +/- 0.25 microU/mg) and 120 min (0.436 +/- 0.35 vs. 0.205 +/- 0.26 microU/mg) (P < 0.05 for all three comparisons). Significant correlations were observed between the daytime period and 24-h average ambulatory systolic blood pressure and the area under the serum insulin curve (r = 0.41 and 0.36, respectively). For non-dippers we found higher fasting insulinaemias but the AUC(insulin) did not differ. Plasma glucose levels did not differ either during fasting or during OGTT (AUC(glucose)). Insulinogenic index was higher in dippers than in non-dippers. We conclude that in lean, postmenopausal hypertensive women insulin resistance is increased compared with age- and weight-matched normotensive women. Also, hyperinsulinaemia correlates with ambulatory systolic blood pressure. Thus, insulin resistance may possibly be involved as a pathogenetic factor in lean, postmenopausal hypertensive women.
 ...
PMID:Insulin resistance and hypertension in postmenopausal women. 1198 14

Diffuse idiopathic skeletal hyperostosis (D.I.S.H.) is a common disorder of unknown aetiology characterized by exuberant hyperostosis of the antero-lateral aspect of the spinal column, that sometimes leads to bone ankilosis, and by ossification of extra-spinal entheses. This condition is often associated with the metabolic derangement of type 2 diabetes. Primary hypertension, its cardiovascular aftereffects and lithiasis are also often present in these patients. D.I.S.H. has to be distinguished from osteoarthritis, although they often coexist in the same patient. The mean difference lies in the anatomical target of the pathological process, that is represented by articular cartilage in osteoarthritis and by entheses in diffuse idiopathic skeletal hyperostosis. The enthesopathy leads to the ossification of the anterior longitudinal ligament of the spine and causes the formation of flowing osteophytes, while intervertebral disc space is quite preserved in early phases of the disease. Symptoms of spine involvement are not typical of the disease and consist of pain and stiffness, usually worsened by inaction and damp. It has also been described the ossification of posterior longitudinal ligament which can lead to medullary canal stenosis. Appendicular skeleton is symmetrically involved in early phases of the disease, the most distinctive affected sites being feet, olecranus and patella. Hip involvement is also frequent and may lead to severe disability and represents an important cause of invalidity. The purpose of the present review is to remark on aetiopathogenetic and clinical aspects of diffuse idiopathic skeletal hyperostosis.
 ...
PMID:[Diffuse idiopathic skeletal hyperostosis (D.I.S.H.)]. 1682 87