Table 1.

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

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.