Insulin resistance in HIV-infected patients: relationship with pro-inflammatory cytokines released by peripheral leukocytes

Objectives. Abnormalities of insulin sensitivity are increasingly reported in HIV infection. Considering that cytokines (particularly TNF-α and IL-1β) can induce insulin resistance in infections, we investigated the relationship between insulin sensitivity and cytokine release from peripheral blood...

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Published in:The Journal of infection Vol. 47; no. 1; pp. 52 - 58
Main Authors: Limone, Paolo, Biglino, Alberto, Valle, Mauro, Degioanni, Maria, Paola Servato, Maria, Berardi, Clara, Del Rizzo, Paola, Pellissetto, Cristina, Carlo Isaia, Giovanni
Format: Journal Article
Language:English
Published: Kidlington Elsevier Ltd 01-07-2003
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Abstract Objectives. Abnormalities of insulin sensitivity are increasingly reported in HIV infection. Considering that cytokines (particularly TNF-α and IL-1β) can induce insulin resistance in infections, we investigated the relationship between insulin sensitivity and cytokine release from peripheral blood mononuclear cells (PBMCs) in HIV-infected patients. Methods. Fourteen HIV-positive patients treated with dual-NRTI (nucleosidic reverse transcriptase inhibitors) regimens, and fourteen healthy controls were studied. Insulin resistance was assessed by homeostatic model for insulin resistance (HOMA-IR). Cytokine production by PBMCs ex vivo was measured. Results. Plasma glucose levels did not differ in HIV patients and in controls. Insulin concentrations and HOMA-IR were significantly higher in HIV-infected patients than in controls (respectively, 11.4±4.3 vs. 7.86±1.1 mIU, P=0.005; 2.27±0.91 vs. 1.6±0.2, P=0.025). A significant positive linear correlation was observed between HOMA-IR and TNF-α concentrations in the supernatants of unstimulated PBMC cultures in HIV patients ( r=0.771; P=0.001 ), but not in controls. Conclusions. Our results are in accordance with previous findings showing that insulin resistance may indeed be present in PI-naive HIV patients, and suggest that either TNF-α, or other mediators released in parallel with this cytokine may induce a state of insulin resistance, unrelated to highly active antiviral treatments, in poorly controlled HIV disease.
AbstractList OBJECTIVESAbnormalities of insulin sensitivity are increasingly reported in HIV infection. Considering that cytokines (particularly TNF-alpha and IL-1beta) can induce insulin resistance in infections, we investigated the relationship between insulin sensitivity and cytokine release from peripheral blood mononuclear cells (PBMCs) in HIV-infected patients. METHODSFourteen HIV-positive patients treated with dual-NRTI (nucleosidic reverse transcriptase inhibitors) regimens, and fourteen healthy controls were studied. Insulin resistance was assessed by homeostatic model for insulin resistance (HOMA-IR). Cytokine production by PBMCs ex vivo was measured. RESULTSPlasma glucose levels did not differ in HIV patients and in controls. Insulin concentrations and HOMA-IR were significantly higher in HIV-infected patients than in controls (respectively, 11.4+/-4.3 vs. 7.86+/-1.1mIU, P=0.005; 2.27+/-0.91 vs. 1.6+/-0.2, P=0.025). A significant positive linear correlation was observed between HOMA-IR and TNF-alpha concentrations in the supernatants of unstimulated PBMC cultures in HIV patients (r=0.771;P=0.001), but not in controls. CONCLUSIONSOur results are in accordance with previous findings showing that insulin resistance may indeed be present in PI-naive HIV patients, and suggest that either TNF-alpha, or other mediators released in parallel with this cytokine may induce a state of insulin resistance, unrelated to highly active antiviral treatments, in poorly controlled HIV disease.
Abnormalities of insulin sensitivity are increasingly reported in HIV infection. Considering that cytokines (particularly TNF-alpha and IL-1beta) can induce insulin resistance in infections, we investigated the relationship between insulin sensitivity and cytokine release from peripheral blood mononuclear cells (PBMCs) in HIV-infected patients. Fourteen HIV-positive patients treated with dual-NRTI (nucleosidic reverse transcriptase inhibitors) regimens, and fourteen healthy controls were studied. Insulin resistance was assessed by homeostatic model for insulin resistance (HOMA-IR). Cytokine production by PBMCs ex vivo was measured. Plasma glucose levels did not differ in HIV patients and in controls. Insulin concentrations and HOMA-IR were significantly higher in HIV-infected patients than in controls (respectively, 11.4+/-4.3 vs. 7.86+/-1.1mIU, P=0.005; 2.27+/-0.91 vs. 1.6+/-0.2, P=0.025). A significant positive linear correlation was observed between HOMA-IR and TNF-alpha concentrations in the supernatants of unstimulated PBMC cultures in HIV patients (r=0.771;P=0.001), but not in controls. Our results are in accordance with previous findings showing that insulin resistance may indeed be present in PI-naive HIV patients, and suggest that either TNF-alpha, or other mediators released in parallel with this cytokine may induce a state of insulin resistance, unrelated to highly active antiviral treatments, in poorly controlled HIV disease.
Objectives. Abnormalities of insulin sensitivity are increasingly reported in HIV infection. Considering that cytokines (particularly TNF-[alpha] and IL-1[beta]) can induce insulin resistance in infections, we investigated the relationship between insulin sensitivity and cytokine release from peripheral blood mononuclear cells (PBMCs) in HIV-infected patients. Methods. Fourteen HIV-positive patients treated with dual-NRTI (nucleosidic reverse transcriptase inhibitors) regimens, and fourteen healthy controls were studied. Insulin resistance was assessed by homeostatic model for insulin resistance (HOMA-IR). Cytokine production by PBMCs ex vivo was measured. Results. Plasma glucose levels did not differ in HIV patients and in controls. Insulin concentrations and HOMA-IR were significantly higher in HIV-infected patients than in controls (respectively, 11.4+/-4.3 vs. 7.86+/-1.1 mIU, P=0.005; 2.27+/-0.91 vs. 1.6+/-0.2, P=0.025). A significant positive linear correlation was observed between HOMA-IR and TNF-[alpha] concentrations in the supernatants of unstimulated PBMC cultures in HIV patients (r=0.771; P=0.001), but not in controls. Conclusions. Our results are in accordance with previous findings showing that insulin resistance may indeed be present in PI-naive HIV patients, and suggest that either TNF-[alpha], or other mediators released in parallel with this cytokine may induce a state of insulin resistance, unrelated to highly active antiviral treatments, in poorly controlled HIV disease.
Objectives. Abnormalities of insulin sensitivity are increasingly reported in HIV infection. Considering that cytokines (particularly TNF-α and IL-1β) can induce insulin resistance in infections, we investigated the relationship between insulin sensitivity and cytokine release from peripheral blood mononuclear cells (PBMCs) in HIV-infected patients. Methods. Fourteen HIV-positive patients treated with dual-NRTI (nucleosidic reverse transcriptase inhibitors) regimens, and fourteen healthy controls were studied. Insulin resistance was assessed by homeostatic model for insulin resistance (HOMA-IR). Cytokine production by PBMCs ex vivo was measured. Results. Plasma glucose levels did not differ in HIV patients and in controls. Insulin concentrations and HOMA-IR were significantly higher in HIV-infected patients than in controls (respectively, 11.4±4.3 vs. 7.86±1.1 mIU, P=0.005; 2.27±0.91 vs. 1.6±0.2, P=0.025). A significant positive linear correlation was observed between HOMA-IR and TNF-α concentrations in the supernatants of unstimulated PBMC cultures in HIV patients ( r=0.771; P=0.001 ), but not in controls. Conclusions. Our results are in accordance with previous findings showing that insulin resistance may indeed be present in PI-naive HIV patients, and suggest that either TNF-α, or other mediators released in parallel with this cytokine may induce a state of insulin resistance, unrelated to highly active antiviral treatments, in poorly controlled HIV disease.
Author Berardi, Clara
Carlo Isaia, Giovanni
Paola Servato, Maria
Biglino, Alberto
Del Rizzo, Paola
Pellissetto, Cristina
Limone, Paolo
Valle, Mauro
Degioanni, Maria
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  surname: Limone
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  surname: Carlo Isaia
  fullname: Carlo Isaia, Giovanni
  organization: Department of Internal Medicine, University of Torino, Torino, Italy
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Issue 1
Keywords HIV infection
insulin resistance
cytokines
Infection
Human
Immunopathology
Target tissue resistance
Leukocyte
Pathogenesis
Viral disease
Cytokine
AIDS
Immune deficiency
Insulin
Language English
License CC BY 4.0
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Snippet Objectives. Abnormalities of insulin sensitivity are increasingly reported in HIV infection. Considering that cytokines (particularly TNF-α and IL-1β) can...
Abnormalities of insulin sensitivity are increasingly reported in HIV infection. Considering that cytokines (particularly TNF-alpha and IL-1beta) can induce...
Objectives. Abnormalities of insulin sensitivity are increasingly reported in HIV infection. Considering that cytokines (particularly TNF-[alpha] and...
OBJECTIVESAbnormalities of insulin sensitivity are increasingly reported in HIV infection. Considering that cytokines (particularly TNF-alpha and IL-1beta) can...
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StartPage 52
SubjectTerms Adult
Biological and medical sciences
Blood Glucose - analysis
cytokines
HIV infection
HIV Infections - blood
HIV Infections - physiopathology
Human viral diseases
Humans
Hydrocortisone - blood
Infectious diseases
Insulin - blood
insulin resistance
Insulin Resistance - physiology
Interleukin-1 - blood
Male
Medical sciences
Tumor Necrosis Factor-alpha - metabolism
Viral diseases
Viral diseases of the lymphoid tissue and the blood. Aids
Title Insulin resistance in HIV-infected patients: relationship with pro-inflammatory cytokines released by peripheral leukocytes
URI https://dx.doi.org/10.1016/S0163-4453(03)00055-0
https://www.ncbi.nlm.nih.gov/pubmed/12850163
https://search.proquest.com/docview/18807240
https://search.proquest.com/docview/73460359
Volume 47
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