Osteocalcin may play a protective role in the pathogenesis of type 2 diabetes, not only through direct involvement in glucose homeostasis, but also through improving lipid profile.

No abstract

INTRODUCTIONPreeclampsia is a clinical manifestation characterized by hypertension, proteinuria and edema that occurs after 20 th week of pregnancy. It is a multisystem disorder of pregnancy with potentially severe consequences for both mother and child.1 It affects about 5-8% of all pregnancies and is a major cause of maternal, fetal and neonatal mortality and morbidity. 2,3 The etiology of preeclampsia is unknown but thought to be related to hypoxia in the placenta and endothelial dysfunction. 4 The various causes that leads to these abnormalities ABSTRACT Background: Preeclampsia affects about 5-8% of all pregnancies and is a major cause of maternal, fetal and neonatal mortality and morbidity. Evidences prove that endothelial cell and altered endothelial cell function play an important role in the pathogenesis of preeclampsia. Therefore serum lactate dehydrogenase (LDH) and serum gamma glutamyl transferase (GGT) are the useful biochemical markers reflecting the severity of the occurrenc e of preeclampsia. The objective was to determine serum lactate dehydrogenase (LDH) and serum gamma glutamyl transferase (GGT) as biochemical markers in preeclamptic pregnant women and its comparison with normal pregnant women in third trimester. Methods: This is the case-control hospital based study carried in the Department of Biochemistry M.G.M. Medical College and associated M.Y. Hospital. Indore (M.P.). Normal pregnant women (n=48), women with preeclampsia (n=53) were included in the study. Both the groups were in their third trimester and of same age and same gestational age. Preeclamptic group was further divided into two subgroups mild (n=36) and severe (n=17) preeclampsia. Results: There were no significant differences among the three groups in age and body mass index but significantly higher differences in gestational age, systolic and diastolic blood pressure was observed. Higher values of serum lactate dehydrogenase (LDH) were found in mild and severe preeclamptic women than those of normal pregnant women in third trimester but the values of serum LDH was significantly elevated in severe preeclamptic women when comparison was done between mild and severe preeclamptic women. Serum GGT was significantly higher among all the groups. Conclusion: Elevated levels of serum LDH and serum GGT indicates the tissue damage related to endothelial vascular damage and are the main cause of the occurrence of preeclampsia.

Genistein, an isoflavonoid phytoestrogen, has been known for its potential pharmacological properties especially for neuroprotection and treating diabetes. The present study aims to determine the neuroprotective efficacy of genistein against global cerebral ischemia-reperfusion-induced neuronal injury in streptozotocin-induced diabetic mice and explore the underlying mechanisms. Streptozotocin-induced diabetic mice were subjected to transient cerebral ischemia by occluding both common carotid arteries for 30 min followed by 24 h reperfusion to induce neuronal injury. Effect of genistein (2.5, 5.0, and 10.0 mg/kg, i.p., o.d.) treatment on ischemia-reperfusion-induced neuronal injury in diabetic mice was evaluated in terms of cerebral infarct size, oxidative damage, mitochondrial activity in terms of neuronal apoptosis and cellular viability, dipeptidyl peptidase-4 activity and active glucagon-like peptide-1 concentration, and neurological functions measured as short-term memory and motor performance. Genistein administration following transient cerebral ischemia significantly (p ˂ 0.0001) counteracted cognitive impairment and re-established (p ˂ 0.001) motor performance in diabetic mice. Ischemia-reperfusion increased the infarct size, genistein administration prevented the increase in cerebral infarct size (p ˂ 0.0001) and significantly suppressed (p ˂ 0.001) the increase in cerebral oxidative stress in transient cerebral ischemia-reperfusion subjected diabetic mice. Genistein treatment significantly (p ˂ 0.001) reduced neuronal apoptosis and increased cellular viability (p ˂ 0.0001), almost completely suppressed (p ˂ 0.0001) the circulating dipeptidyl peptidase-4 activity, and enhanced (p ˂ 0.0001) glucagon-like peptide-1 concentration in diabetic mice with cerebral ischemia-reperfusion. This study suggests that genistein has potent neuroprotective activity against global cerebral ischemia-reperfusion-induced neuronal injury and consequent neurological deficits in streptozotocin-induced diabetic mice.

No abstract