30-year cross-sectional trends in waist-to-height ratio in Australian school age children; 1985 to 2015.

AIM: To report 30-year changes in the proportion of children with abdominal obesity measured by waist-to-height ratio (WHtR) ≥ 0.5. METHODS: Secondary analysis of WHtR ≥ 0.5 data on Australian children age 7 to 15 years from five national cross-sectional population surveys conducted in 1985, 1995, 2007, 2012 and 2015. Changes in the proportions of children with a WHtR ≥ 0.5 across survey years, by age and sex were assessed using chi-squared tests. RESULTS: Between 1985 and 2012, the proportion of children with WHtR ≥ 0.5 increased from 8.6% [95%CI: 8.0, 9.2] to 25.1% [95%CI: 23.5, 26.7]. An increase of ~5% each decade was observed between 1985 and 2007, and a 6.6% increase was observed between 2007 and 2012. Overall, there was a non-significant decrease in the proportion of children with WHtR ≥ 0.5 between 2012 (25.1% [95%CI: 23.5, 26.7] and 2015 (23.3% [95%CI: 21.6, 25.2]. CONCLUSION: Abdominal obesity has increased over the last 30 years in Australian children. In 2015, one in five children had WHtR ≥ 0.5, a marker of cardiometabolic risk in children. Our finding highlights the importance of including WHtR as a routine measurement in primary health care and population health surveys. This information is needed to guide policy and practice to manage long-term cardiovascular risk in children.

Molecular mechanisms of lipid metabolism disorder in livers of ewes with pregnancy toxemia.

Pathogenesis of pregnancy toxemia (PT) is believed to be associated with the disruption of lipid metabolism. The present study aimed to explore the underlying mechanisms of lipid metabolism disorder in the livers of ewes with PT. In total, 10 pregnant ewes were fed normally (control group) whereas another 10 were subjected to 70% level feed restriction for 15 days to establish a pathological model of PT. Results showed that, as compared with the controls, the levels of blood ß-hydroxybutyrate (BHBA), non-esterified fatty acids (NEFAs) and cholesterol were greater (P<0.05) and blood glucose level was lower (P<0.05) in PT ewes. The contents of NEFAs, BHBA, cholesterol and triglyceride were higher (P<0.05) and glycerol content was lower (P<0.05) in hepatic tissues of PT ewes than those of the controls. For ewes with PT, excessive fat vacuoles were observed in liver sections stained with hematoxylin-eosin; furthermore, inner structures of hepatocytes including nuclei, mitochondria and endoplasmic reticulum were damaged seriously according to the results of transmission electron microscope. Real-time PCR data showed that compared with the controls, the expression of hepatic genes involved in fatty acid oxidation (FAO) and triglyceride synthesis (TGS) was enhanced (P<0.05) whereas that related to acetyl-CoA metabolism (ACM) was repressed (P<0.05) in PT ewes. Generally, our results showed that negative energy balance altered the expression of genes involved in FAO, ACM and TGS, further caused lipid metabolism disorder in livers, resulting in PT of ewes. Our findings may provide the molecular basis for novel therapeutic strategies against this systemic metabolic disease in sheep.

Expression of aquaporin 1 and 4 in rats with acute hypoxic lung injury and its significance.

Aquaporin (AQP)-1 and AQP-4 expression in lung tissues of SD rats during high altitude hypoxic lung injury, and the relationship between AQP-1 and AQP-4 expression, and acute hypoxic lung injury was analyzed. Thirty six healthy SD rats were divided into hypoxia 1d, 2d, 3d, 5d, and 7d groups and control group (N = 6). Pathological changes in lung tissue were observed by hematoxylin and eosin staining; lung injury was scored, and ultrastructural changes in lung tissue were observed by transmission electron microscopy. Changes in moisture content in lung tissues were determined by analyzing the wet/dry weight ratio (W/D). Localization of AQP-1 and AQP-4 was determined by immunohistochemistry. AQP-1 and AQP-4 expression were detected by western blot. Lung W/D was lower in hypoxia groups than in control group, and the highest in 3d group (P < 0.05). Light microscopy revealed a thickening alveolar wall and outstretched and congestive alveolar wall in hypoxia group; electron microscopy revealed the presence of abnormal alveolar type II epithelial cells, cavitation in cytoplasm, microvillus-like protrusions, and a reduced lamellar body. AQP- 1 and AQP-4 were mainly distributed in the capillaries and lymphatic and alveolar epithelial cells and airway epithelial cells, respectively. AQP-1 protein expression was decreased (western blot) in hypoxia 1d group (the lowest in 3d group; P < 0.05); there were no significant changes about AQP- 4 expression. Therefore, AQP-1 may be involved in abnormal transport of liquid ALI and pathogenesis of lung edema. AQP-4 may not be involved in the formation of ALI lung edema.