Insulin resistance (IR) is the condition in which normal amounts of insulin are inadequate to produce a normal insulin response from fat, muscle and liver cells. Insulin resistance in fat cells reduces the effects of insulin and results in elevated hydrolysis of stored triglycerides in the absence of measures which either increase insulin sensitivity or which provide additional insulin.
Increased mobilization of stored lipids in these cells elevates free fatty acids in the blood plasma. Insulin resistance in muscle cells reduces glucose uptake (and so local storage of glucose as glycogen), whereas insulin resistance in liver cells results in impaired glycogen synthesis and a failure to suppress glucose production.
Elevated blood fatty-acid concentrations (associated with insulin resistance and diabetes mellitus Type 2), reduced muscle glucose uptake, and increased liver glucose production all contribute to elevated blood glucose concentration. High plasma levels of insulin and glucose due to insulin resistance are believed to be the origin of metabolic syndrome and type 2 diabetes, including its complications.
Several associated conditions include:
- Abnormally Sedentary lifestyle, whether the result of the effects of aging on the body or lack of physical exercise (both of which can also produce obesity)
- Tobacco Smoking
- Coffee (A Canadian study has found that consumption of caffeine makes insulin more resistant to alterations in blood sugar in patients with and without diabetes.)
- Polycystic ovarian syndrome (PCOS)
- Hypercortisolism (e.g., steroid use or Cushing's disease)
- Drugs (e.g., rifampicin, isoniazid, olanzapine, risperidone, progestogens, corticosteroids, glucocorticoids, many antiretrovirals, possibly alcohol, methadone)
- Genetic causes
- Insulin receptor mutations (Donohue Syndrome)
- LMNA mutations (Familial Partial Lipodystrophy)
Insulin resistance may also be caused by the damage of liver cells having undergone a defect of insulin receptors in hepatocytes.
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