Insulin resistance has been linked to diabetes, hypertension, dyslipidemia and cardiovascular disease. Obesity is a common thread among metabolic disorders (Reilly an Rader 2003) as well as cardiovascular disease (Haffner 1997; Lempiainen, Mykkanen et al. 1999) and is associated with insulin resistance.(Goodpaster, Thaete et al. 1997) In addition to generalized obesity by either body fat or body mass index (BMI) criteria, insulin resistance is also associated with the distribution of body fat, including abdominal visceral fat (Goodpaster, Thaete et al. 1997) and fat accumulation within skeletal muscle.(Goodpaster, Thaete et al. 2000) There is also increasing evidence that impaired capacity for fat oxidation in obesity and type 2 diabetes is related to insulin resistance (Kelley, Goodpaster et al. 1999) Thus, the metabolic disturbances of insulin resistance and type 2 diabetes appear to be more global to include dysregulated fat metabolism as well as impaired glucose metabolism.
The alarming increase in obesity in the U.S. (Mokdad, Ford et al. 2003) and around the world (Hernandez, Cardonnet et al. 1987; al-Isa 1995; Hodge, Dowse et al. 1995; Flegal, Carroll et al. 1998; Arroyo, Loria et al. 2000) is a paramount public health concern affecting children, middle-aged and older men and women across a variety of ethnic and racial groups. The increase in obesity has led to a marked increase in the metabolic syndrome (Ford, Giles et al. 2002) creating additional risks for type II diabetes and cardiovascular disease. Data from the Framingham study have established an increased incidence of cardiovascular events with increasing weight (Hubert, Feinleib et al. 1983; Colditz, Willett et al. 1995) and weight gain was a significant risk factor for development of diabetes. The association of obesity with the insulin resistance syndrome is not only related to the degree of obesity but is dependent on body fat distribution. Thus, individuals with greater degrees of central adiposity develop this syndrome more frequently than do those with a peripheral body fat distribution.(Kissebah and Krakower 1994).
CONTENTS
PREFACE
- 1.0 INTRODUCTION
1.1 OBESITY
1.2 BIPOLAR DISORDER
- 1.2.1 Primary Specific Aims
2.0 SECOND CHAPTER
2.1 LITERATURE REVIEW
- 2.1.1 BACKGROUND
2.2 BIPOLAR DISORDER
2.3 METABOLIC SYNDROME
- 2.3.1 Metabolic Syndrome in Bipolar Disorder
2.4 INSULIN RESISTANCE
- 2.4.1 Insulin Resistance in Bipolar Disorder
2.5 OBESITY
- 2.5.1 Obesity in Bipolar Disorder
2.5.2 Causes of Obesity in Bipolar Disorder
2.5.3 Central Obesity
2.5.4 Central Obesity in Bipolar Disorder
2.6 SKELETAL MUSCLE FATTY ACID METABOLISM
2.6.1 Mechanisms
2.7 MEDICATIONS IN BIPOLAR DISORDER
- 2.7.1 Antidepressants
2.7.2 Monoamine oxidase inhibitors (MAOI)
2.7.3 Tricyclic Antidepressants
2.7.4 Selective Serotonin Reuptake Inhibitors (SSRI)
2.7.5 Atypical Antipsychotics
3.0 CHAPTER 3
3.1 METHODS
- 3.1.1 Subjects
3.1.2 Bipolar Patients
3.1.3 Controls:
3.2 EXPERIMENTAL DESIGN AND METHODS
- 3.2.1 Screening Procedures
3.2.2 Physical Activity Measurement (Following Visit 1):
3.2.3 Visit 2
3.3 DATA ANALYSES
4.0 CHAPTER 4
4.1 RESULTS
- 4.1.1 Subjects
4.1.2 Insulin Resistance
4.1.3 Metabolic Characteristics
4.2 OBESITY
- 4.2.1 Whole Body Fat and Lean Mass
4.2.2 Regional Fat Distribution
4.3 ENERGY EXPENDITURE:
4.4 FATTY ACID METABOLISM
4.5 NUTRITION BEHAVIOR
5.0 CHAPTER 5
5.1 DISCUSSION
- 5.1.2 Insulin Resistance
5.2 OBESITY
- 5.2.1 Generalized Obesity
5.2.2 Regional Fat Distribution
5.3 ENERGY EXPENDITURE
5.4 FATTY ACID METABOLISM
5.5 NUTRITION BEHAVIOR
5.6 SUMMARY AND CONCLUSIONS
5.7 LIMITATIONS AND FUTURE DIRECTION
APPENDIX A: INFORMED CONSENT
APPENDIX B: BASELINE DEMOGRAPHIC AND MEDICAL HISTORY FORM
BIBLIOGRAPHY
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Obesity, Body Composition and Insulin Resistance in Women With And Without Bipolar Disorder
