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The cytokine Interleukin 6 and C-reactive protein are common inflammatory markers used to diagnose systemic inflammation risk. [3] Baseline C-reactive protein levels deviate due to natural genetic variation, but significant increases can result from risk factors such as smoking, obesity, lifestyle, and high blood pressure. [3]
The Dietary Inflammatory Index (DII) is a numerical score that assesses a diet for its effect on several biomarkers linked to inflammation.Its theoretical bounds are −8.87 to +7.98, and it is oriented such that negative scores are more anti-inflammatory and more positive scores are pro-inflammatory.
C-reactive protein (CRP) is an annular (ring-shaped) pentameric protein found in blood plasma, whose circulating concentrations rise in response to inflammation. It is an acute-phase protein of hepatic origin that increases following interleukin-6 secretion by macrophages and T cells .
The connecting peptide, or C-peptide, is a short 31-amino-acid polypeptide that connects insulin's A-chain to its B-chain in the proinsulin molecule. In the context of diabetes or hypoglycemia, a measurement of C-peptide blood serum levels can be used to distinguish between different conditions with similar clinical features.
High-sensitivity C-reactive protein has been developed and used as a marker to predict coronary vascular diseases in metabolic syndrome, and it was recently used as a predictor for nonalcoholic fatty liver disease (steatohepatitis) in correlation with serum markers that indicated lipid and glucose metabolism. [58]
In this article, all values (except the ones listed below) denote blood plasma concentration, which is approximately 60–100% larger than the actual blood concentration if the amount inside red blood cells (RBCs) is negligible.
C-reactive protein (CRP) is an acute phase protein. Therefore, it is a better marker for acute phase reaction than ESR. While ESR and CRP generally together correlate with the degree of inflammation, this is not always the case and results may be discordant [9] in 12.5% of the cases. [7]
The glucose tolerance test was first described in 1923 by Jerome W. Conn. [4]The test was based on the previous work in 1913 by A. T. B. Jacobson in determining that carbohydrate ingestion results in blood glucose fluctuations, [5] and the premise (named the Staub-Traugott Phenomenon after its first observers H. Staub in 1921 and K. Traugott in 1922) that a normal patient fed glucose will ...