Skip to main content

Table 1 History of insulin resistance from different perspectives of research in the fields of diabetology, infection/inflammation, pain, mental activation, trauma, and rheumatology.

From: Insulin resistance, selfish brain, and selfish immune system: an evolutionarily positively selected program used in chronic inflammatory diseases

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]
  1. 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.