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

1916

Joslin

Hyperglycemia in infectious diseases,^a painful gallstones,^b trauma^c

1920

Pemberton and Foster

Impaired glucose regulation in soldiers with arthritis^a

1924

Rabinowitch

Enormous doses of insulin needed in infected diabetic patients^a

1929

Root

IR in the context of different diseases^a,b,c

1936

Himsworth and Kerr

Insulin-sensitive and insulin-insensitive diabetes

1938

Thomsen

Traumatic diabetes^c

1938

Warren

β-cell defects in older longstanding diabetic patients

1950

Liefmann

IR in rheumatoid arthritis (combined glucose and insulin test)^a

1956

Arendt and Pattee

IR in obese subjects

1957

Collins

IR in schizophrenia^d

1960

Yalow and Berson

IR in diabetic subjects (high glucose despite high insulin)

1963

Randle and colleagues

Fatty acids support IR

1965

van Praag and Leijnse

Major depression induces IR^d

1965

Butterfield and Wichelow

Forearm insulin sensitivity test

1970

Shen and colleagues

Quadruple insulin sensitivity test

1979

DeFronzo and colleagues

Euglycemic insulin clamp technique in combination with radioisotope turnover, limb catheterization, indirect calorimetry, and muscle biopsy

1979

Wolfe

Review: sepsis and trauma induce IR^a,b,c

1982

Kasuga and colleagues

Insulin induces tyrosine phosphorylation of the insulin receptor

1982

Ciraldi and colleagues

Reduced insulin-stimulated glucose uptake in type 2 diabetes

1984

Grunberger and colleagues

Dissociation between normal insulin binding and defective tyrosine kinase activity of the insulin receptor

1986

Garvey and colleagues

Hyperinsulinemia induces insulin receptor desensitization

1987

Svenson and colleagues

IR in rheumatoid arthritis^a

1988

Krieger and Landsberg

Hypertension, hyperinsulinemia, insulin resistance and SNS

1988

DeFronzo

Hyperglycemia decreases glucose transport and inhibits beta-cell function (glucotoxicity)

1988

DeFronzo, Reaven

Increased free fatty acids play key role in IR, β-cell dysfunction, and hepatic gluconeogenesis (lipotoxicity)

1988

Uchita and colleagues, Greisen and colleagues

Pain influences IR via the HPA axis and SNS^b

1992

Feingold and Grunfeld

Cytokines like TNF play a role in hyperlipidemia and diabetes^a

1993

Hotamisligil and colleagues

TNF critically influences IR^a

1994

Moberg and colleagues

Mental stress induces acute IR in type 1 diabetic patients^d

1996

Keltikangas and colleagues

Mental stress is accompanied by IR in nondiabetic people^d

1999

Björntrop

IR as a consequence of exaggerated HPA axis and SNS activation (CNS stress is the trigger)^d

2000

Chrousos

Mental stress-induced hypercortisolism induces IR (the pseudo-Cushing state)^d

2000

Seematter and colleagues

Mental stress acutely increases insulin-stimulated glucose utilization in healthy lean humans but not in obese nondiabetic humans^d

2004

Tso and colleagues

Patients with systemic lupus erythematosus demonstrate IR independent of autoantibodies to insulin receptor^a

2005

Kiortsis and colleagues, Stagakis and colleagues

Patients with ankylosing spondylitis and rheumatoid arthritis have IR, which is reduced after anti-TNF therapy^a

2007

Larsen and colleagues

IL-1ra improved beta-cell secretory function in type 2 diabetic patients (no influence on IR)^e

2008

Fleischman and colleagues, Goldfine and colleagues

Salsalate improved insulin sensitivity in young obese adults and in type 2 diabetic patients

2010

Schultz and colleagues

Patients with rheumatoid arthritis show IR, which can be reduced by blocking IL-6^a

2012, 2014

DIAGRAM and colleagues, Fall and Ingelsson

Human gene polymorphisms link both inflammation and metabolic disease