Metabolic Syndrome Pathophysiology: The Role of Essential Fatty AcidsMetabolic Syndrome Pathophysiology: The Role of Essential Fatty Acids provides current research exploring the links among insulin, insulin receptors, polyunsaturated fatty acids, brain growth and disease. Specific interactions of essential fatty acids and polyunsaturated fatty acids in brain development and several disease groups are described. The role of inflammation in disease and how fatty acids regulate low-systemic inflammation are examined and explained. Metabolic and neurologic dynamics are presented to provide a linkage between the presence of omega-3 and omega-6 and protection against diseases and conditions such as diabetes mellitus, obesity, autoimmune diseases and hypertension. |
Contents
Insulin Resistance in the Metabolic Syndrome | 13 |
Is It Necessary to Redefine the Metabolic Syndrome? | 22 |
CONTENTS | 34 |
Obesity | 43 |
Perinatal Nutrition and Obesity | 74 |
Essential Hypertension | 86 |
Dietary Factors and Hypertension | 105 |
Is Hypertension a Disorder of the Brain? | 113 |
Insulin and Insulin Receptors in the Brain and Their Role in | 146 |
Insulin Endothelial Nitric Oxide | 156 |
Obesity Type 2 Diabetes Mellitus the Metabolic Syndrome and | 167 |
Is It Possible That the Metabolic Syndrome Originates in | 177 |
Role of EFAsPUFAs in Brain Growth and Development | 201 |
EFAsPUFAs and Their Metabolites in Insulin Resistance | 240 |
EFAsPUFAs and Atherosclerosis | 252 |
| 265 | |
Type 2 Diabetes Mellitus | 122 |
Pathophysiology of Type 2 Diabetes Mellitus with Particular | 130 |
Other editions - View all
Metabolic Syndrome Pathophysiology: The Role of Essential Fatty Acids Undurti N. Das Limited preview - 2009 |
Metabolic Syndrome Pathophysiology: The Role of Essential Fatty Acids Undurti N. Das No preview available - 2010 |
Common terms and phrases
actions activity adipose tissue adult alterations animals associated BDNF blood pressure body brain cause cells changes Clin compared concentrations decrease diabetes mellitus diet dietary disease dopamine dysfunction effect elevated endothelial energy enhanced essential et al exercise expression factor fatty acids food intake function gene glucose growth heart higher human hypertension hypothalamic impaired important increased indicate induced inflammation inflammatory inhibition insulin receptor insulin resistance interaction leads lean leptin levels lipid liver mediated metabolic syndrome METABOLIC SYNDROME PATHOPHYSIOLOGY mice modulate monoamines mRNA muscle neurons neuropeptide nitric oxide normal noted Nutrition obesity observation occur pancreatic pathway patients perilipin peripheral Physiol plasma play prevent production protein PUFAs rats reduced regulation release reported response risk role secretion seen sensitivity serotonin showed signaling significant significantly stimulation studies subjects suggesting supported suppress sympathetic synthase synthesis type 2 diabetes various vascular weight whereas