Risk factors There are a number of risk factors for<unk> , including being overweight or obese or having a sedentary lifestyle. Various genetic factors can increase risk, such as a family history of diabetes, and there are some specific medical conditions associated with<unk> , such as polycystic ovary syndrome. The National Institute of Diabetes and Digestive and Kidney Diseases states that specific risks that may predispose an individual to<unk>  can include: * being aged 45 or older * having African American, Alaska Native, American Indian, Asian American, Hispanic/Latino, Native Hawaiian, or Pacific Islander American ethnicity * having health conditions such as high blood pressure and abnormal cholesterol levels * having a history of gestational diabetes * having a history of heart disease or stroke. In addition some medications and other health conditions can raise the risk. Lifestyle factors Dietary factors likely contribute to<unk> , however, causative foods are difficult to determine given the limitations of nutrition research. Foods that have independently been linked to<unk>  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. Overconsumption of fat- and sugar-rich meals and beverages have been proposed as a fundamental factor behind the metabolic syndrome epidemic. Diet also has the potential to change the ratio of polyunsaturated to saturated phospholipids in cell membranes. The percentage of polyunsaturated fatty acids (PUFAs) is inversely correlated with<unk> . It is hypothesized that increasing cell membrane fluidity by increasing PUFA concentration might result in an enhanced number of insulin receptors, an increased affinity of insulin to its receptors, and reduced<unk> . Vitamin D deficiency has also been associated with<unk> . Sedentary lifestyle increases the likelihood of development of<unk> . In epidemiological studies, higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Studies have consistently shown that there is a link between<unk>  and circadian rhythm, with insulin sensitivity being higher in the morning and lower in the evening. A mismatch between the circadian rhythm and the meals schedule, such as in circadian rhythm disorders, may increase<unk> . Medications Some medications are associated with<unk>  including corticosteroids, protease inhibitors (type of HIV medication), and atypical antipsychotics. Hormones Many hormones can induce<unk>  including cortisol, growth hormone, and human placental lactogen. Cortisol counteracts insulin and can lead to increased hepatic gluconeogenesis, reduced peripheral utilization of glucose, and increased<unk> . It does this by decreasing the translocation of glucose transporters (especially GLUT4) to the cell membrane. Based on the significant improvement in insulin sensitivity in humans after bariatric surgery and rats with surgical removal of the duodenum, it has been proposed that some substance is produced in the mucosa of that initial portion of the small intestine that signals body cells to become insulin resistant. If the producing tissue is removed, the signal ceases and body cells revert to normal insulin sensitivity. No such substance has been found as yet, and the existence of such a substance remains speculative. Leptin is a hormone produced from the ob gene and adipocytes. Its physiological role is to regulate hunger by alerting the body when it is full. Studies show that lack of leptin causes severe obesity and is strongly linked with<unk> . Diseases Polycystic ovary syndrome and non-alcoholic fatty liver disease (NAFLD) are associated with<unk> . Hepatitis C also makes people three to four times more likely to develop type 2 diabetes and<unk> . Inflammation Acute or chronic inflammation, such as in infections, can cause<unk> . TNF-α is a cytokine that may promote<unk>  by promoting lipolysis, disrupting insulin signaling, and reducing the expression of GLUT4. Genetics Several genetic loci have been determined to be associated with insulin insensitivity. This includes variation in loci near the NAT2, GCKR, and IGFI genes associated with<unk> . Further research has shown that loci near the genes are linked to<unk> . However, these loci are estimated to only account for 25-44% of the genetic component of<unk> .
Insulin resistance
Alpha cell hyperplasia
Hyperinsulinism
Sarcopenic obesity
Hypoestrogenism
Reactive hypoglycemia
Thyroid hormone resistance
Abnormal basal metabolic rate