For just over a decade, much attention has been dedicated to the relationship between inflammation and metabolism, and researchers have come up with some interesting findings. For example, under- or malnourished individuals tend to be immunosuppressed1, while overweight or obese individuals are at a greater risk of inflammatory-related diseases. Adipose tissue is an active endocrine organ that can contribute to the inflammatory process. Adiponectin is produced exclusively by adipocytes and is reduced with obesity. Low levels of adiponectin induced by obesity are thought to contribute to impaired endothelial function, vascular reactive oxygen species formation, and atherogenesis2.
Resistin is another adipocytokine thought to contribute to inflammation, linking obesity to insulin resistance. It upregulates adhesion molecules. Elevated insulin levels are associated with obesity and insulin resitance3. VCAM-1 and MCP-1 and lower levels of resistin are associated with better outcomes following percutaneous coronary intervention4. Resistin also can exert effects through the PI3K/Akt pathway and may be involved directly in cardiovascular disease and indirectly in nutritional regulation2.
Leptin is thought to be mostly released into the blood from the fat cells composing adipose tissue, but it can also be released by lymphocytes5.
The well-studied cytokine TNF-α has been shown to be expressed in the adipose tissue and muscle of humans and rodents with elevated expression in those who are obese6. TNF-α contributes to insulin resistance, or a diminished response to a given amount of insulin, possibly through reducing insulin-mediated insulin receptor autophosphorylation7.
PAI-1, IL-8, IL-10, and CRP are all elevated with obesity5. IL-1 and IL-6 have also been associated with the development of type 2 diabetes8,9. IL-1β is also thought to be a paracrine regulator in adipose tissue . IL-6 (and its soluble receptor) are increased as a result of exercise10, a well known inhibitor of insulin resistance11. Studies have shown that the individual cytokines do not seem to exert individual effects but the combinations of the cytokines do12.
Adiponectin, Leptin, Insulin, IL-1α, IL-1β, IL-6, IL-8, IL-10, MCP-1, PAI-1, TNF-alpha, and CRP
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- Wellen KE, Hotamisligil GS: Inflammation, stress, and diabetes. J Clin Invest 2005, 115:1111-1119.
- Wang Z, Nakayama T: Inflammation, a link between obesity and cardiovascular disease. Mediators Inflamm 2010, 2010:5359181.
- Steinberger J, Daniels SR: Obesity, insulin resistance, diabetes, and cardiovascular risk in children: an American Heart Association scientific statement from the Atherosclerosis, Hypertension, and Obesity in the Young Committee (Council on Cardiovascular Disease in the Young) and the Diabetes Committee (Council on Nutrition, Physical Activity, and Metabolism). Circulation 2003, 107:1448-1453.
- Momiyama Y, Ohmori R, Uto-Kondo H, Tanaka N, Kato R, Taniguchi H, Arakawa K, Nakamura H, Ohsuzu F: Serum Resistin Levels and Cardiovascular Events in Patients Undergoing Percutaneous Coronary Intervention. J Atheroscler Thromb 2010.
- Fain JN: Release of inflammatory mediators by human adipose tissue is enhanced in obesity and primarily by the nonfat cells: a review. Mediators Inflamm 2010, 2010:513948.
- Saghizadeh M, Ong JM, Garvey WT, Henry RR, Kern PA: The expression of TNF alpha by human muscle. Relationship to insulin resistance. J Clin Invest 1996, 97:1111-1116.
- Hotamisligil GS, Arner P, Caro JF, Atkinson RL, Spiegelman BM: Increased adipose tissue expression of tumor necrosis factor-alpha in human obesity and insulin resistance. J Clin Invest 1995, 95:2409-2415.
- Kristiansen OP, Mandrup-Poulsen T: Interleukin-6 and diabetes: the good, the bad, or the indifferent? Diabetes 2005, 54 Suppl 2:S114-124.
- Thomas HE, Irawaty W, Darwiche R, Brodnicki TC, Santamaria P, Allison J, Kay TW: IL-1 receptor deficiency slows progression to diabetes in the NOD mouse. Diabetes 2004, 53:113-121.
- Gray SR, Robinson M, Nimmo MA: Response of plasma IL-6 and its soluble receptors during submaximal exercise to fatigue in sedentary middle-aged men. Cell Stress Chaperones 2008, 13:247-251.
- Pauli JR, Cintra DE, Souza CT, Ropelle ER: [New mechanisms by which physical exercise improves insulin resistance in the skeletal muscle]. Arq Bras Endocrinol Metabol 2009, 53:399-408.
- Spranger J, Kroke A, Mohlig M, Hoffmann K, Bergmann MM, Ristow M, Boeing H, Pfeiffer AF: Inflammatory cytokines and the risk to develop type 2 diabetes: results of the prospective population-based European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam Study. Diabetes 2003, 52:812-817.