Hyperglycaemia
obesity, Adiposity, adiposity, MADD, hyperglycaemia
OBESITY, ADIPOSITY, MULTIPLE ACYL-COA DEHYDROGENASE DEFICIENCY, ADIPOSITY, HYPERGLYCAEMIA
Maternal hyperglycaemia was associated with increased lipid abundance in maternal blood and increased carnitines in cord blood. There are several main sources of fatty acids in maternal blood: (1) dietary intake; (2) lipogenesis; and (3) lipolysis, which are all dynamically regulated by human pregnancy but produce a different fatty acid profile in serum. Dietary data suggest that serum lipid abundance is not related to a maternal high-fat diet (ESM Tables Carnitines were abundant in cord blood in association with maternal hyperglycaemia and adiposity. Carnitines are essential cofactors required for the transportation of long-chain fatty acids into the mitochondrion for β oxidation, the process of generating ATP from fatty acids, typically active in states of low glucose availability. This is a surprising finding, as our current understanding of early human metabolism suggests that the fetus is entirely reliant on glycolysis as a means of fuel production, with β oxidation ‘switched on’ after birth, once the infant metabolism has to adjust to fasting. Inherited or acquired defects in fatty acid oxidation cause increases in the abundance of carnitines and present from day 3 of life, not from birth (for example, C4-C18:1 acylcarnitines in multiple acyl-CoA dehydrogenase deficiency [MADD]) [Adiposity in offspring was associated with carnitines and abundant lipid species with lipogenesis-related fatty acids. β oxidation and de novo lipogenesis do not usually run concurrently but can do so, for example, as described in adults with obesity or after over-feeding, where an energy-consuming cycle of β oxidation and de novo lipogenesis is likely to reduce excess fuel from excess calories [