Metabolic
 Liza Phillips
Adiponectin - role in modulating postprandial inflammatory, metabolic and cardiovascular stress
Background
The incidence and health care costs of obesity, type 2 diabetes (T2DM) and non-alcoholic-fatty liver disease (NAFLD) are increasing rapidly. Inflammation and oxidative stress are implicated in insulin resistance and cardiovascular disease. Increasing evidence suggests the postprandial state promotes this inflammatory milieu.
In addition to the nutrient induced inflammation and oxidative stress, postprandial hyperglycaemia and hyperlipidaemia are associated with endothelial dysfunction and a hypercoagulable state.
Adiponectin, an anti-inflammatory, insulin-sensitising hormone, is synthesised primarily in adipose tissue, and circulates in high levels in various multimeric structures. High molecular weight (HMW) adiponectin appears to be most metabolically active. Hypoadiponectinaemia has been implicated in the pathogenesis of T2DM and NAFLD. Emerging evidence suggests that postprandial inflammation, oxidative stress and hyperglycaemia alter adiponectin secretion and multimeric distribution.
There is limited and conflicting information regarding postprandial adiponectin levels and, to our knowledge, postprandial adiponectin multimeric distribution has not been evaluated.
Hypothesis
- Adiponectin multimer distribution is altered postprandially such that HMW adiponectin increases in lean-healthy subjects, and decreases in those with metabolic dysfunction (T2DM, obesity and NAFLD).
- HMW adiponectin modifies the inflammatory response to a meal, decreasing postprandial inflammation, oxidative stress, coagulability and endothelial dysfunction.
Aim
- To measure baseline and postprandial adiponectin concentration and multimer distribution in the study cohorts.
- To correlate baseline and postprandial adiponectin profiles with inflammatory and oxidative stress markers, coagulation measures and vascular function in the studied cohorts.
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