Table 1.
Year | Author | Phenomena | Reference |
---|---|---|---|
1916 | Joslin | Hyperglycemia in infectious diseases,a painful gallstones,b traumac | [1] |
1920 | Pemberton and Foster | Impaired glucose regulation in soldiers with arthritisa | [2] |
1924 | Rabinowitch | Enormous doses of insulin needed in infected diabetic patientsa | [3] |
1929 | Root | IR in the context of different diseasesa,b,c | [4] |
1936 | Himsworth and Kerr | Insulin-sensitive and insulin-insensitive diabetes | [106] |
1938 | Thomsen | Traumatic diabetesc | [107] |
1938 | Warren | β-cell defects in older longstanding diabetic patients | In [108] |
1950 | Liefmann | IR in rheumatoid arthritis (combined glucose and insulin test)a | [16] |
1956 | Arendt and Pattee | IR in obese subjects | [109] |
1957 | Collins | IR in schizophreniad | [110] |
1960 | Yalow and Berson | IR in diabetic subjects (high glucose despite high insulin) | [24] |
1963 | Randle and colleagues | Fatty acids support IR | [25] |
1965 | van Praag and Leijnse | Major depression induces IRd | [111] |
1965 | Butterfield and Wichelow | Forearm insulin sensitivity test | [112] |
1970 | Shen and colleagues | Quadruple insulin sensitivity test | [113] |
1979 | DeFronzo and colleagues | Euglycemic insulin clamp technique in combination with radioisotope turnover, limb catheterization, indirect calorimetry, and muscle biopsy | [114] |
1979 | Wolfe | Review: sepsis and trauma induce IRa,b,c | [115] |
1982 | Kasuga and colleagues | Insulin induces tyrosine phosphorylation of the insulin receptor | [116] |
1982 | Ciraldi and colleagues | Reduced insulin-stimulated glucose uptake in type 2 diabetes | [117] |
1984 | Grunberger and colleagues | Dissociation between normal insulin binding and defective tyrosine kinase activity of the insulin receptor | [118] |
1986 | Garvey and colleagues | Hyperinsulinemia induces insulin receptor desensitization | [119] |
1987 | Svenson and colleagues | IR in rheumatoid arthritisa | [17] |
1988 | Krieger and Landsberg | Hypertension, hyperinsulinemia, insulin resistance and SNS | [120] |
1988 | DeFronzo | Hyperglycemia decreases glucose transport and inhibits beta-cell function (glucotoxicity) | [121] |
1988 | DeFronzo, Reaven | Increased free fatty acids play key role in IR, β-cell dysfunction, and hepatic gluconeogenesis (lipotoxicity) | [121,122] |
1988 | Uchita and colleagues, Greisen and colleagues | Pain influences IR via the HPA axis and SNSb | [123,124] |
1992 | Feingold and Grunfeld | Cytokines like TNF play a role in hyperlipidemia and diabetesa | [125] |
1993 | Hotamisligil and colleagues | TNF critically influences IRa | [34] |
1994 | Moberg and colleagues | Mental stress induces acute IR in type 1 diabetic patientsd | [126] |
1996 | Keltikangas and colleagues | Mental stress is accompanied by IR in nondiabetic peopled | [127] |
1999 | Björntrop | IR as a consequence of exaggerated HPA axis and SNS activation (CNS stress is the trigger)d | [28] |
2000 | Chrousos | Mental stress-induced hypercortisolism induces IR (the pseudo-Cushing state)d | [29] |
2000 | Seematter and colleagues | Mental stress acutely increases insulin-stimulated glucose utilization in healthy lean humans but not in obese nondiabetic humansd | [128] |
2004 | Tso and colleagues | Patients with systemic lupus erythematosus demonstrate IR independent of autoantibodies to insulin receptora | [19] |
2005 | Kiortsis and colleagues, Stagakis and colleagues | Patients with ankylosing spondylitis and rheumatoid arthritis have IR, which is reduced after anti-TNF therapya | [20,44] |
2007 | Larsen and colleagues | IL-1ra improved beta-cell secretory function in type 2 diabetic patients (no influence on IR)e | [129] |
2008 | Fleischman and colleagues, Goldfine and colleagues | Salsalate improved insulin sensitivity in young obese adults and in type 2 diabetic patients | [43,130] |
2010 | Schultz and colleagues | Patients with rheumatoid arthritis show IR, which can be reduced by blocking IL-6a | [45] |
2012, 2014 | DIAGRAM and colleagues, Fall and Ingelsson | Human gene polymorphisms link both inflammation and metabolic disease | [93,131] |
CNS, central nervous system; DIAGRAM, DIAbetes Genetics Replication And Meta-analysis Consortium; HPA, hypothalamic-pituitary-adrenal; IL, interleukin; IR, insulin resistance; OGTT, oral glucose tolerance test; SNS, sympathetic nervous system; TNF, tumor necrosis factor. aInsulin resistance as a consequence of infection or inflammation. bInsulin resistance as a consequence of pain. cInsulin resistance as a consequence of trauma. dInsulin resistance as a consequence of mental activation. eApproved by the US Food and Drug Administration for patients with type 2 diabetes mellitus.