Obesity and cardiovascular disease is common in bipolar disorder, both of which are associated with insulin resistance. Insulin resistance is also associated with distribution of body fat, specifically abdominal visceral fat and fat accumulation in skeletal muscle. Furthermore, reduced capacity to utilize fat has been linked with obesity, type 2 diabetes and insulin resistance. PURPOSE: To compare insulin sensitivity, body composition and resting substrate utilization between obese and normal weight patients with bipolar 1 disorder and race, age and BMI matched controls. METHODS: Participants underwent dual energy X-ray absorptiometry (DEXA) to measure fat mass (FM) and fat-free mass (FFM), computed tomography (CT) to measure cross-sectional abdominal adipose tissue and indirect calorimetry to measure resting substrate oxidation. Free- living energy expenditure was measured for 5 days using BodyMedia SenseWear Pro Armband and the food frequency questionnaire estimated the usual consumption of 79 main food items over the preceding 12 months. Insulin sensitivity was measured from fasting insulin and glucose measurements and defined by the homeostatic model assessment of insulin resistance (HOMA IR). RESULTS: Eighteen patients with bipolar 1 disorder and 17 controls participated in this study. There were no differences observed in insulin resistance between obese (BMI > 30 kg/m2) patients and controls (56.8 ± 17.2 vs. 51.8 ± 11.1; P = 0.842) or normal weight (BMI < 25 kg/m2) patients and controls (30.5 ± 6.3 vs. 27.0 ± 5.7 P = 0.691). CT revealed a difference in total abdominal fat (718.1 ± 33.6 vs. 607.4 ± 38.6cm2; P = 0.04), a trend in visceral abdominal fat (P = 0.06) though no difference in subcutaneous abdominal fat between obese patients and controls. Indirect calorimetry revealed a trend (P=0.06) in reduced fat oxidation in normal weight patients compared to controls and when combining obese and normal weight patients. CONCLUSION: Patients with bipolar 1 disorder do not appear to be more insulin resistant than controls after accounting for their obesity. However, a reduced fat oxidation in normal weight patients may be an underlying factor predisposing them for future weight gain and concomitant increased risk for type 2 diabetes.
| Identifer | oai:union.ndltd.org:PITT/oai:PITTETD:etd-12082006-105612 |
| Date | 30 January 2007 |
| Creators | Fleet, Sara Beth |
| Contributors | Andreas Fagiolini, M.D., Bret H. Goodpaster, Ph.D., John J Jakicic, Ph.D., Amy Otto, Ph.D., David Kupfer, M.D. |
| Publisher | University of Pittsburgh |
| Source Sets | University of Pittsburgh |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://etd.library.pitt.edu/ETD/available/etd-12082006-105612/ |
| Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to University of Pittsburgh or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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