relationship between body mass index [BMI] and pregnancy complications including mode of delivery

To study the impact of prepregnancy BMI on the mode of delivery. We wish to test the hypothesis that a raised BMI in the first trimester predicts a higher rate of medical complications and operative deliveries. This is a prospective observational study of women delivering at the Women's Hospital during January and February 2005. Of 340 primigravidas who delivered during that period we included sixty in the study using exclusion criteria such as booking after the first trimester and multiple pregnancies. The authors collected data; a sheet was used and then entered in the computer. The obstetric outcomes looked into by means of SPSS statistical package. Both overweight and obese patients showed a higher pregnancy complication rate as compared to those of normal prepregnancy BMI. Glucose intolerance [25% in the obese Vs 15%in the normal BMI group]. Hypertension was 8.3% in the obese vs. 0% in the normal BM1 group. Obstetric interventions were also significantly higher in the High BMI group. Induction of labour was 31% in the obese group compared to 15% in the normal BMI group, prolonged second stage was 56% in the obese versus 37% in the normal BMI group, Caesarean section [CS] was 46% in the overweight women and 33% in the obese vs. 20% in the normal BMI group. Fetal macrosomia was 12.5% in the obese compared to a zero percent in the normal BMI group. The rate of prematurity was significantly reduced in the obese] 0% vs. 15% [n=3] in the normal BMI group with 26.7% [n=4] in the overweight.] A high BMI may be an indicator of risk for the pregnancy and delivery

Uncoupling protein 3 andhypothalamic neuropeptide yexpression in response todietary fat in rats

Objective:Obesity results when energy intake is greater than energyexpenditure. Skeletal muscles [SK.M] UCP3 and central NPY play an im-portant role in energy balance. The aim is to study the changes of [SK.M]UCP3 expression, and hypothalamic NPYmRNA expression after pro-longed feeding with high-fat diet [HFD]

Design:Obese-prone Sprague Dawley rats were fed beef tallow[46%] of energy as fat "HFD" and control group fed libitum diets contain-ing 4.5% of energy as fat [control], for 16 weeks. Body weight and foodintake were measured every 3 days throughout the experimental period.After the feeding period is completed, hindlimb skeletal muscle was iso-lated for subsequent determinations of triglyceride. Skeletal UCP3 mRNAand hypothalamic NPY mRNA were assessed by [RT-PCR] respectively

Results:Plasma glucose, triglyceride, insulin, leptin and free fatty ac-ids levels were higher in rats fed the HFD compared to control group. HFDresulted in significant increase in [SK.M] triglyceride, and mRNA levels of[SK.M] UCP3 by [3.84 folds], but without significant change in hypotha-lamic NPY mRNA expression compared to control group

Conclusion:high fat diet induces obesity with marked induction ofUCP3. The dissociation between the UCP3 mRNA levels and NPY mRNAexpression could point that obesity may be caused by mechanisms inde-pendent of thermogensis

Effect of leptin on renal functions in rabbits

The aim of this work is to evaluate the hemodynamic changes of leptin administration to rabbits. A total of 18 male New Zealand rabbits, weighing from 1 to 1.5 kg were included in this study. After induction of anesthesia, basal arterial blood pressure [Am, sodium [Na+], potassium [K+] and creatinine concentrations in both blood and urine samples were evaluated. The animals were then randomly assigned to 3 groups of 6 each. Group I [control] received isotonic saline by intravenous infusion. Group II [study group] received intra-arterial injection of leptin [10 micro g/kg] for one Hour followed by a 10-Jold higher dose of leptin. Group III [negative control] received intravenous bolus injection of propranolol [0.1 mg] for one hour followed by a similar dose for the next hour. Administration of leptin resulted in slight increase in mean arterial pressure [MAP] that reached significance after 90 min and persisted above the basal level for the recording period of 2 hours. There were no parallel changes, at either doses, infraction reabsorption of Na+, K+, H20 and glomerular filtration rate [GFR] as compared to both basal values and to control animals. It was concluded that the elevation in MAP induced by leptin was most probably not related to renal mechanism, as there were no significant changes in renal parameters studied. This suggests another mechanism for the rise in MAP, a suggestion which needs further studies