Type of Document Master's Thesis Author Sarjeant, Kelesha Crystal Author's Email Address email@example.com URN etd-06172011-090919 Title The Expression of Cardiotrophin-1 Is Differentially Regulated in Murine and Human Obesity Type II Diabetes Degree Master of Science (M.S.) Department Biochemistry (Biological Sciences) Advisory Committee
Advisor Name Title Stephens, Jacqueline M. Committee Chair Bartlett, Sue G. Committee Member DiMario, Patrick Committee Member Keywords
- insulin resistance
- western blotting
Date of Defense 2011-06-08 Availability unrestricted AbstractCardiovascular disease is the leading cause of mortality in all developed nations. Several independent studies have shown that cardiotrophin-1 (CT-1) serum levels are modulated in patients with various types of cardiovascular disease including ischemic heart disease, valvular heart disease, and accelerated arthrosclerosis. CT-1 is a member of the Interleukin-6 family, or gp130 family of cytokines. It is also known to induce cardiomyocyte hypertrophy in vitro and in vivo, and is a critical component for cardiomyocyte survival. CT-1 is a naturally occurring protein with a molecular mass of approximately 21.5 kD and a 200 amino acid long sequence, it was discovered in a cDNA screen of murine stem cells and was originally identified in cardiomyocytes. Since then, CT-1 expression has been reported in several other tissues including skeletal muscle, liver, ovary, kidney and lung.
Interestingly, our studies reveal that CT-1 protein expression is significantly modulated in adipose tissue following high fat feeding in C57BL/6 mice. Of note, we did not observe regulation of CT-1 expression in white adipose tissue in human obesity and Type II Diabetes Mellitus (T2DM). We can readily detect CT-1 in the media of cultured adipocytes. This study suggests that CT-1 secretion from murine adipose tissue may be an important contributor to the levels of circulating CT-1. In summary, our studies demonstrate that CT-1 is an adipokine that is modulated in murine obesity and T2DM.
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