Key result
Long-standing and newly diagnosed pediatric diabetes show distinct plasma lipid patterns without reported quantitative differences.
Why the study?
The lipid disturbances consequent on lack of insulin in juvenile diabetes and their potential role in vascular disease development were not fully characterized in diabetic children.
Observational
Answers are grounded in this paper and cite their sources.
No quantitative lipid data reported; leaves open any differences in diabetic children and should not inform practice.
Adipose tissue represents a major source of high energy fuel and allows for the expenditure of enercgy for long periods between feedings. The lipid present in fat tissue has a potentially high turnover rate, is metabolically active and responsive both to the needs of the individual and to the hormonal milieu of the tissue. The major hormone involved in lipogenesis, and which inhibits lipolysis, is insulin.' Lipid and carbohydrate metabolism are interdependent, and the lipid disturbance consequent on lack of insulin in juvenile diabetes may be as profound as the abnormalities of glucose metabolism. Plasma levels of free fatty acids are markedly elevated in untreated juvenile diabetes. This is probably entirely accounted for by increased breakdown of adipose triglyceride when, as with insulin lack, lipolysis is increased and re-esterification is decreased. In addition, concentrations of catecholamines, growth hormone and glucagon, which stimulate hormone sensitive lipase activity, may rise in ketoacidosis. The raised levels of free fatty acids released into the circulation arc largely metabolised in thc liver, where uptake is not influenced by insulin lack. On uptake, free fatty acids are esterified to triglyceride, and in diabetes the extent of triglyceride synthesis in liver appears to be largely determined by plasma free-fatty-acid concentration. Other consequences of disturbance of lipid metabolism in untreated juvenile diabetes include increased formation of the organic acids, beta-hydroxybutyric and acetoacetic acid with a subsequent formation of acetone. Cholesterol concentration in plasma may also rise in association with the other lipid consequences of insulin lack. Travia (1971) showed a correlation between lipid and cholesterol concentration in blood and impaired glucosc tolerance. There is interest in the possible role of diabetic hyperlipaemia in the development of vascular disease (Lloyd et al., 1962). We have, thereforc, studied plasma lipid patterns in diabetic children, comparing newly diagnosed children with those with long-standing disease.
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Court et al. (1978) conducted an observational in Juvenile diabetes. Newly diagnosed diabetes vs. Long-standing diabetes was evaluated on Plasma lipid patterns. The abstract describes a study comparing plasma lipid patterns between newly diagnosed and long-standing diabetic children, but reports no quantitative results.
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