Aims: The present study was undertaken to explore the relationship of plasma homocysteine in the pathogenesis of neuropathy in diabetic patients. Subjects and Methods: Forty two type 2 diabetic patients [22 with neuropathy (DN group) and 20 without neuropathy (DNN group)], age range between 35-70 years had relatively controlled glycemia and duration of diabetes 7-15 years, were studied. Motor and sensory nerve conduction velocities and action potential amplitudes of peripheral nerves were determined by following standard protocol. HbA1c was estimated by modified HPLC (BIO-RAD Variant, USA). Serum C-peptide was measured by enzyme linked immunosorbentassay (ELISA), plasma total homocysteine by Fluorescent Polarization Immunoassay (FPIA). Results: Age, BMI and blood pressure of the study subjects were. Duration of diabetes between DN and DNN groups was comparable. DN group had significantly higher fasting glucose levels (9.8±3.8, mmol/l) compared to the DNN group (6.9±1.8, p=0.004). This trend was also reflected in the HbA1c level: 8.7± 2.1 vs 7.2±1.6 in DN group and DNN group respectively (p=0.009). The two diabetic groups had relatively higher absolute C-peptide level compared to the controls (p=ns). DN and DNN groups had significantly higher plasma homocysteine level compared to the Controls. But between the two diabetic groups no significant difference was observed. Ulnar and peroneal motor nerve conduction velocities and compound muscle action potentials in the diabetic neuropathy group significantly lower compared to diabetic counterpart and the controls. Ulnar and sural sensory nerve conduction velocities and action potentials were significantly lower in the diabetic neuropathy group compared to the diabetic counterpart and the controls. Plasma homocysteine did not show any correlation with nerve conduction velocities and action potential amplitudes. Conclusions: The data concluded that (i) Diabetic neuropathy may not be related to hyperhomocysteinemia in type 2 diabetic patients of Bangladeshi origin; (ii) Hyperglycemia, even at milder level, is related to neuronal dysfunction in these subjects; and (ii) Hyperinsulinemia don't seem to be prerequisite for neuropathy in these subjects.
Background and Aims: Cord blood leptin may reflect the leptinemic status of a newborn at birth more accurately than the leptin values of blood collected from other sites. The present study was undertaken to determine the relationship of cord serum leptin concentration at birth with neonatal and maternal anthropometric parameters. Materials and Methods: Blood was taken from the umbilical cord of the babies at delivery. Maternal anthropometric measurements were recorded at admission for delivery. Neonatal anthropometric measurements were recorded within 48 hours after delivery. Linear regression analysis was used to explore the relationship between cord serum leptin concentration and anthropometric parameters of the baby and the mother. Both Serum leptin and serum C-peptide levels were measured by chemiluminescence-based ELISA method. Results: The leptin concentration (ng/ml, mean±SD) in cord blood was 39.13±14.44. Cord leptin levels correlated with birth weight (r=0.673, p<0.0001), ponderal index (r=0.732, p<0.0001) but it did not correlate with maternal body mass index, gestational age (r=0.135, p=0.349) at delivery or cord serum C-peptide concentration (r=-0.049, p=0.735) or placental weight (r=0.203, p=0.157). Conclusion: There are associations between cord leptin concentration at delivery and birth weight, ponderal index (PI) of the babies but not body mass index (BMI) of the mothers. High leptin levels of the baby could represent an important feedback modulator of substrate supply and subsequently for adipose tissue status during late gestation. (J Bangladesh Coll Phys Surg 2007; 25 : 9-13)
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.