Effects of calcium/calmodulin kinase and high-fat feeding on weight gain and insulin action / by Robert R. Fish.
| Author/creator | Fish, Robert R. author. |
| Other author | Dohm, G. Lynis, degree supervisor. |
| Other author | Kalmus, Gerhard W., degree supervisor. |
| Other author | East Carolina University. Department of Biology. |
| Format | Theses and dissertations |
| Production | 2004. |
| Description | 60 leaves : illustrations ; 28 cm |
| Supplemental Content | Access via ScholarShip |
| Subjects |
| Summary | Calcium-calmodulin dependent protein kinase (CaM Kinase) is a signaling protein involved in the programming of skeletal muscle fiber type. CaM Kinase activation promotes a fiber-type transition from white, fast-twitch, predominantly glycolytic, type lEB muscle fibers, to red slow-twitch, oxidative types I and IIA fibers. Oxidative fibers are more insulin sensitive and exhibit increased rates of glucose uptake and disposal. Therefore, increasing the proportion of red fiber-types may have therapeutic applications for the treatment of patients with type II diabetes. Muscle is the major site of glucose disposal in the body and muscle from type II diabetic individuals shows decreased insulin-stimulated glucose disposal. Since insulin-stimulated glucose disposal is proportional to the relative amounts of slow-twitch fibers, a fiber-type switch from a white to a red fiber phentoype, promoted by CaM Kinase, is a possible target for improving glucose disposal in insulin resistant individuals. Through the use of transgenic mice expressing a constitutively active form of CaM Kinase (CAMK*), this study investigated the effects of CAMK* activation on animal weight, fat pad weight, muscle weight, rate of glycogen synthesis and insulin signaling on CAMK* and wild-type (WT) mice. Since a high-fat diet causes insulin resistance, we also fed WT and CAMK* mice a high-fat diet to investigate whether the CAMK* protein could protect against insulin resistance and weight gain. Wild-type mice gained 10% more weight (p[less-than]0.01) on the high-fat diet, but the body weight of the CAMK* mice was not increased by high-fat feeding. The glucose disposal analysis presented conflicting results. The CAMK* protein had no clear effect on glycogen synthesis rate. High-fat diet caused a significant decrease in tyrosine phosphorylated ER (p[less-than]0.05) and IRS-1 (p[less-than]0.01) of WT mice but not CAMK* mice. Overall, the CAMK* protein conferred resistance to weight gain following high-fat feeding and a decreased susceptibility to high-fat diet induced depression of insulin signal transduction. |
| General note | Presented to the faculty of the Department of Biology. |
| General note | Advisor: G. Lynis Dohm. |
| General note | Advisor: Gerhard W. Kalmus |
| Dissertation note | M.S. East Carolina University 2004 |
| Bibliography note | Includes bibliographical references (leaves 56-60). |
| Genre/form | Academic theses. |
| Genre/form | Academic theses. |
| Genre/form | Thèses et écrits académiques. |
Availability
| Library | Location | Call Number | Status | Item Actions |
|---|---|---|---|---|
| Joyner | University Archives | ASK AT SPECIAL COLLECTIONS DESK | ✔ Available | Request Material |
| Electronic Resources | ✔ Available |