The influence of angiotensin II and RAAS blockers on lipolytic and glycolytic activity in isolated adipocytes from Wistar, Wistar-Kyoto and Spontaneously Hypertensive Rats.

The renin-angiotensin-aldosterone system (RAAS) is related to dysfunctional adipose tissue, but the actions of angiotensin II (AII) in adipocytes remains unclear. This study aimed to investigate the effects of RAAS blockers and AII in lipolysis and glycolysis from isolated adipocytes in Wistar (WIS), Wistar-Kyoto (WKY) and Spontaneously Hypertensive Rats (SHR). Adipocytes from 15-weeks-old WIS, WKY and SHR were incubated with AII (10-17 M to 10-6 M) and noradrenaline (NOR - 10-10 M to 10-4 M) in presence or not of antagonists (Losartan Potassium 10-4 M, PD 123319 5.6 nM or co-incubation). Glycerol and lactate production in WIS and WKY were not affected by the RAAS blockade. SHR glycerol was attenuated by the blockers but lactate was not affected. NOR induced increase in glycerol from 10-7 M for all strains. Normotensive rats are not affected by blockers but decreased lipolytic activity ins SHR. The SHR hypolipodistrophy cannot be related to any disturbance in lipolytic or glycolytic upstream pathways.

The influence of hypertensive environment on adipose tissue remodeling measured by fluorescence lifetime imaging in spontaneously hypertensive rats.

There is a lack of information correlating low adiposity with hypertension experienced by Spontaneous Hypertensive Rats (SHR) or overweight and normotension in Wistar-Kyoto (WKY). We aimed to investigate this lipodystrophy phenomenon by measuring fluorescence lifetime (FLIM), optical redox ratio (ORR), serum levels of hypothalamic-pituitary-adrenal (HPA) and/or hypothalamic-pituitary-thyroid (HPT) hormones axes between Wistar, WKY and SHR before and after establishment of hypertension. Under high blood pressure, we evaluated serum adipokines. Brown adipose tissue was characterized as lower ORR and shorter FLIM compared to white adipose tissue. HPT axis showed a crucial role in the SHR adipose tissue configuration by attenuating whitening. The increased adiposity in WKY may act as a preventive agent for hypertension, since SHR, with low adiposity, establishes the disease. The hypertensive environment can highlight key adipokines that may result in new therapeutic approaches to the treatment of adiposity dysfunctions and hypertension.

Dietary leucine supplementation minimises tumour-induced damage in placental tissues of pregnant, tumour-bearing rats.

BACKGROUND: The occurrence of cancer during pregnancy merges two complex, poorly understood metabolic and hormonal conditions. This association can exacerbate the conditions of both the mother and the foetus. The branched-chain amino acid leucine enhances cellular activity, particularly by increasing protein synthesis. This study aimed to analyse the modulatory effect of a leucine-rich diet on direct and indirect tumour-induced placental damage. This was accomplished by evaluating the expression of genes involved in protein synthesis and degradation and assessing anti-oxidant enzyme activity in placental tissues collected from pregnant, tumour-bearing rats. RESULTS: Pregnant rats were either implanted with Walker 256 tumour cells or injected with ascitic fluid (to study the indirect effects of tumour growth) and then fed a leucine-rich diet. Animals in a control group underwent the same procedures but were fed a normal diet. On the 20(th) day of pregnancy, tumour growth was observed. Dams fed a normoprotein diet showed the greatest tumour growth. Injection with ascitic fluid mimicked the effects of tumour growth. Decreased placental protein synthesis and increased protein degradation were observed in both the tumour-bearing and the ascitic fluid-injected groups that were fed a normoprotein diet. These effects resulted in low placental DNA and protein content and high lipid peroxidation (measured by malondialdehyde content). Decreased placental protein synthesis-related gene expression was observed in the tumour group concomitant with increased expression of genes encoding protein degradation-associated proteins and proteolytic subunits. CONCLUSIONS: Consumption of a leucine-rich diet counteracted the effects produced by tumour growth and injection with ascitic fluid. The diet enhanced cell signalling, ameliorated deficiencies in DNA and protein content, and balanced protein synthesis and degradation processes in the placenta. The improvements in cell signalling included changes in the mTOR/eIF pathway. In conclusion, consumption of a leucine-rich diet improved placental metabolism and cell signalling in tumour-bearing rats, and these changes reduced the deleterious effects caused by tumour growth.