Regional Brazilian diet-induced pre-natal malnutrition in rats is correlated with the proliferation of cultured vascular smooth muscle cells.

OBJECTIVES: Pre-natal malnutrition induces hypertension and insulin resistance, pathologies commonly linked to atherosclerotic disease. The proliferation of vascular smooth muscle cells (SMCs) is important during development of the atherosclerotic plaque. In this work, we investigated whether the serum of pre-natal malnourished Wistar rats could alter the proliferation of aortic and renal artery SMCs in culture. Malnutrition was induced by feeding a basic regional diet available in a rural area of Pernambuco State, Brazil. This diet was rich in carbohydrates and deficient in proteins, lipids, vitamins and minerals, including sodium chloride. METHODS AND RESULTS: Serum was obtained from the blood of 90-day-old control and pre-natal undernourished rats. SMCs from control Wistar rats at the 6th passage were allowed to adhere to plates in Dulbecco's modified Eagle's medium (DMEM) supplemented with fetal calf serum (10%). Subsequently, the SMCs were maintained in DMEM supplemented with rat serum (10%). The number of cells was counted on the 3rd, 6th and 8th days of culture into rat serum. [3H]-thymidine incorporation into SMCs was evaluated after 20 h or 6 days of incubation. The birth weight of male and female undernourished offspring was 25% (p<0.05) and 46% (p<0.05) lower, respectively, than their corresponding control groups. On the 8th day of culture, the number of aortic SMCs in the serum of undernourished male and female rats, as well as renal artery SMCs in the serum of undernourished female rats, was higher than in the serum of control rats. The [3H]-thymidine incorporation was higher in aortic SMCs incubated for 6 days in the serum of undernourished male and female rats. At confluence, the density of aortic SMCs was higher than that of renal artery SMCs. CONCLUSIONS: Pre-natal malnutrition produces serum with altered properties that can affect the proliferation of SMCs and may contribute to atherosclerotic disease.

Cord blood essential fatty acid and alpha-tocopherol in full-term newborns in a Northeast Brazil area.

Malnutrition of children during the first two years of life constitutes a public health concern in Brazil, particularly in the Northeast. Most of the nutrition data are concerned with protein-energy malnutrition and hypovitaminosis A. The purpose of this cross-sectional study was to assess the essential fatty acid (EFA) status, which is crucial in physical and mental development, and that of vitamin E which prevents against the oxidative loss of EFA physiological properties, in 81 full-term newborns. Blood samples were obtained from the residual blood of the umbilical cord (UC) at delivery. Fatty acid composition of UC plasma did not show any sign of EFA deficiency. The levels of docosahexanoic (DHA) and arachidonic acid (AA) appeared to be quite similar to those obtained in European populations. UC plasma vitamin E content was 6.31 +/- 1.99 mumol/L whereas the lipid-normalized vitamin E was 2.36 mumol/mmol of lipids. An interesting point was that newborns with vitamin E inferior to the median value (5.80 mumol/L) revealed significantly lower contents of linoleic acid and DHA in UC than newborns superior to the median value. Together with the absolute or normalized plasma level of vitamin E, this supports the observation that one quarter of the community's newborns is deficient in vitamin E.

Renal effects of essential fatty acid deficiency in hydropenic and volume-expanded rats.

The aim of this paper was to study the effects of essential fatty acid (EFA) on fractional sodium excretion (FE(Na(+))) and renal hemodynamics in rats during hydropenia (H) and acute volume expansion (VE), successively. Mean arterial pressure (MAP) and renal blood flow (RBF) were measured using a blood pressure transducer and a flow probe, respectively, both connected to a flowmeter. Glomerular filtration rate (GFR) was estimated by inulin clearance. The rats receiving coconut oil as only source of dietary lipids (the EFA-deficient group) presented lower levels of linoleic acid in cortex and medulla and lower body weight than the rats receiving soy oil in place of coconut oil (the control non-EFA-deficient group). During H, the EFA-deficient rats exhibited a lower level of renal vascular resistance resulting in a higher level of RBF and a higher urinary flow (V') and FE(Na(+)), although GFR was lower than in the control group. During VE, the rats of the control group responded with increased MAP, RBF, V' and FE(Na(+)), which were not found in the EFA-deficient group, suggesting an impaired hemodynamic adjustment in EFA deficiency. In conclusion, both experimental conditions revealed that EFA deficiency affects the renal hemodynamics.