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P Hlavatý

Publications and source records attributed to P Hlavatý.

At least 19 recordsLinked to original sources

[Acylation stimulating protein--its role in control of metabolism in the adipose tissue].

Multiple hormones and enzymes participate in the lipid storage. One of them is acylation stimulating protein. Acylation stimulating protein is produced predominantly by adipocytes. After the binding on specific receptor at the surface of adipocytes, acylation stimulating protein leads to enhancement of triglyceride synthesis. This process is mediated by protein-kinase C. Concurrently, glucose transporters move from the cytoplasm to the adipocyte surface. Higher glucose disposal leads to a sufficient substrate availability for triglyceride synthesis. Acylation stimulating protein also stimulates pancreatic insulin secretion. Total acylation stimulating protein level in plasma is related to the adipose tissue mass and it positively correlates with many anthropometric parameters and with serum insulin level. In acylation stimulating protein deficient mice, resistance to the obesity development after a high fat diet was observed. Adipose tissue mass is lower in the acylation stimulating protein deficient mice and higher insulin sensitivity was shown in acylation stimulating protein deficient mice compared to a wild type mice. Acylation stimulating protein pathway may have an important role in the obesity development.

Adipose Tissue↗

The influence of n-3 polyunsaturated fatty acids and very low calorie diet during a short-term weight reducing regimen on weight loss and serum fatty acid composition in severely obese women.

Polyunsaturated fatty acids of n-3 series (n-3 PUFA) were shown to increase basal fat oxidation in humans. The aim of the study was to compare the effect of n-3 PUFA added to a very low calorie diet (VLCD), with VLCD only during three-week inpatient weight reduction. Twenty severely obese women were randomly assigned to VLCD with n-3 PUFA or with placebo. Fatty acids in serum lipid fractions were quantified by gas chromatography. Differences between the groups were determined using ANOVA. Higher weight (7.55+/-1.77 vs. 6.07+/-2.16 kg, NS), BMI (2.82+/-0.62 vs. 2.22+/-0.74, p<0.05) and hip circumference losses (4.8+/-1.81 vs. 2.5+/-2.51 cm, p<0.05) were found in the n-3 group as compared to the control group. Significantly higher increase in beta-hydroxybutyrate was found in the n-3 group showing higher ketogenesis and possible higher fatty acid oxidation. The increase in beta-hydroxybutyrate significantly correlated with the increase in serum phospholipid arachidonic acid (20:4n-6; r = 0.91, p<0.001). In the n-3 group significantly higher increase was found in n-3 PUFA (eicosapentaenoic acid, 20:5n-3, docosahexaenoic acid, 22:6n-3) in triglycerides and phospholipids. The significant decrease of palmitoleic acid (16:1n-7) and vaccenic acid (18:1n-7) in triglycerides probably reflected lower lipogenesis. A significant negative correlation between BMI change and phospholipid docosahexaenoic acid change was found (r = -0.595, p<0.008). The results suggest that long chain n-3 PUFA enhance weight loss in obese females treated by VLCD. Docosahexaenoate (22:6n-3) seems to be the active component.

3-Hydroxybutyric Acid↗