Insulin resistance is a pathological condition in which cells fail to respond normally to the hormone insulin.
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Insulin resistance is a pathological condition in which cells fail to respond normally to the hormone insulin.
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Insulin resistance is released by the pancreas in response to carbohydrates consumed in the diet.
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Risk factors for insulin resistance include obesity, sedentary lifestyle, family history of diabetes, various health conditions, and certain medications.
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Insulin resistance is considered a component of the metabolic syndrome.
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Insulin resistance can be improved or reversed with lifestyle approaches, such as exercise and dietary changes.
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Foods that have independently been linked to insulin resistance include those high in sugar with high glycemic indices, high in dietary fat and fructose, low in omega-3 and fiber, and which are hyper-palatable which increases risk of overeating.
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Some medications are associated with insulin resistance including corticosteroids, protease inhibitors, and atypical antipsychotics.
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Many hormones can induce insulin resistance including cortisol, growth hormone, and human placental lactogen.
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Insulin resistance is strongly associated with intestinal-derived apoB-48 production rate in insulin-resistant subjects and type 2 diabetic patients.
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Insulin resistance often is found in people with visceral adiposity, hypertension, hyperglycemia, and dyslipidemia involving elevated triglycerides, small dense low-density lipoprotein particles, and decreased high-density lipoprotein cholesterol levels.
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The result of NAFLD is an excessive release of free fatty acids into the bloodstream, and an increase in hepatic breakdown of glycogen stores into glucose, both of which have the effect of exacerbating peripheral insulin resistance and increasing the likelihood of Type 2 diabetes mellitus.
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Also, insulin resistance often is associated with a hypercoagulable state and increased inflammatory cytokine levels.
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Insulin resistance has been proposed to be a reaction to excess nutrition by superoxide dismutase in cell mitochondria that acts as an antioxidant defense mechanism.
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Gold standard for investigating and quantifying insulin resistance is the "hyperinsulinemic euglycemic clamp, " so-called because it measures the amount of glucose necessary to compensate for an increased insulin level without causing hypoglycemia.
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The authors caution against demeaning the importance of Insulin resistance and combined exercise, as this type of training is generally less researched than aerobic training.
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Concept that insulin resistance may be the underlying cause of diabetes mellitus type 2 was first advanced by Professor Wilhelm Falta and published in Vienna in 1931, and confirmed as contributory by Sir Harold Percival Himsworth of the University College Hospital Medical Centre in London in 1936; however, type 2 diabetes does not occur unless there is concurrent failure of compensatory insulin secretion.
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Evidence is contradictory to Neel in studies of the Pima Indians, which indicate that the people with higher insulin sensitives tended to weigh the most and conversely people with insulin resistance tended to weigh less on average in this demographic.
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