Defective glucose and lipid metabolism in human immunodeficiency virus-infected patients with lipodystrophy involve liver, muscle tissue and pancreatic beta-cells.

Steen B Haugaard; Ove Andersen; Flemming Dela; Jens Juul Holst; Heidi Storgaard; Mogens Fenger; Johan Iversen; Sten Madsbad; Steen B Haugaard; Ove Andersen; Flemming Dela; Jens Juul Holst; Heidi Storgaard; Mogens Fenger; Johan Iversen; Sten Madsbad

Defective glucose and lipid metabolism in human immunodeficiency virus-infected patients with lipodystrophy involve liver, muscle tissue and pancreatic beta-cells.

Bidragets oversatte titel: Defective glucose and lipid metabolism in human immunodeficiency virus-infected patients with lipodystrophy involve liver, muscle tissue and pancreatic beta-cells.

Steen B Haugaard, Ove Andersen, Flemming Dela, Jens Juul Holst, Heidi Storgaard, Mogens Fenger, Johan Iversen, Sten Madsbad, Steen B Haugaard, Ove Andersen, Flemming Dela, Jens Juul Holst, Heidi Storgaard, Mogens Fenger, Johan Iversen, Sten Madsbad

Abstract

OBJECTIVES: Lipodystrophy and insulin resistance are prevalent among human immunodeficiency virus (HIV)-infected patients on combined antiretroviral therapy (HAART). Aiming to provide a detailed description of the metabolic adverse effects of HIV-lipodystrophy, we investigated several aspects of glucose metabolism, lipid metabolism and beta-cell function in lipodystrophic HIV-infected patients. METHODS: [3-3H]glucose was applied during euglycaemic hyperinsulinaemic clamps in association with indirect calorimetry in 43 normoglycaemic HIV-infected patients (18 lipodystrophic patients on HAART (LIPO), 18 patients without lipodystrophy on HAART (NONLIPO) and seven patients who were naive to antiretroviral therapy (NAIVE) respectively). beta-cell function was evaluated by an intravenous glucose tolerance test. RESULTS: Compared with NONLIPO and NAIVE separately, LIPO displayed markedly reduced ratio of limb to trunk fat (RLF; > 34%, P < 0.001), hepatic insulin sensitivity (> 40%, P < 0.03), incremental glucose disposal (>50%, P < 0.001) and incremental exogenous glucose storage (>50%, P < 0.05). Furthermore, LIPO displayed reduced incremental glucose oxidation (P < 0.01), increased clamp free fatty acids (P < 0.05) and attenuated insulin-mediated suppression of lipid oxidation (P < 0.05) compared with NONLIPO. In combined study groups, RLF correlated with hepatic insulin sensitivity (r = 0.69), incremental glucose disposal (r = 0.71) and incremental exogenous glucose storage (r = 0.40), all P < 0.01. Disposition index (i.e. first-phase insulin response to intravenous glucose multiplied by incremental glucose disposal) was reduced by 46% (P = 0.05) in LIPO compared with the combined groups of NONLIPO and NAIVE, indicating an impaired adaptation of beta-cell function to insulin resistance in LIPO. CONCLUSION: Our data suggest that normoglycaemic lipodystrophic HIV-infected patients display impaired glucose and lipid metabolism in multiple pathways involving liver, muscle tissue and beta-cell function.

Bidragets oversatte titel	Defective glucose and lipid metabolism in human immunodeficiency virus-infected patients with lipodystrophy involve liver, muscle tissue and pancreatic beta-cells.
Originalsprog	Engelsk
Tidsskrift	European Journal of Endocrinology
Vol/bind	152
Udgave nummer	1
Sider (fra-til)	103-112
Antal sider	10
ISSN	0804-4643
Status	Udgivet - 2005

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http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15762193&query_hl=3

Citationsformater

Haugaard, S. B., Andersen, O., Dela, F., Holst, J. J., Storgaard, H., Fenger, M., Iversen, J., Madsbad, S., Haugaard, S. B., Andersen, O., Dela, F., Holst, J. J., Storgaard, H., Fenger, M., Iversen, J., & Madsbad, S. (2005). Defective glucose and lipid metabolism in human immunodeficiency virus-infected patients with lipodystrophy involve liver, muscle tissue and pancreatic beta-cells. European Journal of Endocrinology, 152(1), 103-112. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15762193&query_hl=3

Defective glucose and lipid metabolism in human immunodeficiency virus-infected patients with lipodystrophy involve liver, muscle tissue and pancreatic beta-cells. / Haugaard, Steen B; Andersen, Ove ; Dela, Flemming et al.

I: European Journal of Endocrinology, Bind 152, Nr. 1, 2005, s. 103-112.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

Haugaard, SB, Andersen, O , Dela, F , Holst, JJ, Storgaard, H, Fenger, M, Iversen, J, Madsbad, S, Haugaard, SB, Andersen, O, Dela, F, Holst, JJ, Storgaard, H, Fenger, M, Iversen, J & Madsbad, S 2005, 'Defective glucose and lipid metabolism in human immunodeficiency virus-infected patients with lipodystrophy involve liver, muscle tissue and pancreatic beta-cells.', European Journal of Endocrinology, bind 152, nr. 1, s. 103-112. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15762193&query_hl=3>

@article{d02ec0405f2f11dea8de000ea68e967b,

title = "Defective glucose and lipid metabolism in human immunodeficiency virus-infected patients with lipodystrophy involve liver, muscle tissue and pancreatic beta-cells.",

abstract = "OBJECTIVES: Lipodystrophy and insulin resistance are prevalent among human immunodeficiency virus (HIV)-infected patients on combined antiretroviral therapy (HAART). Aiming to provide a detailed description of the metabolic adverse effects of HIV-lipodystrophy, we investigated several aspects of glucose metabolism, lipid metabolism and beta-cell function in lipodystrophic HIV-infected patients. METHODS: [3-3H]glucose was applied during euglycaemic hyperinsulinaemic clamps in association with indirect calorimetry in 43 normoglycaemic HIV-infected patients (18 lipodystrophic patients on HAART (LIPO), 18 patients without lipodystrophy on HAART (NONLIPO) and seven patients who were naive to antiretroviral therapy (NAIVE) respectively). beta-cell function was evaluated by an intravenous glucose tolerance test. RESULTS: Compared with NONLIPO and NAIVE separately, LIPO displayed markedly reduced ratio of limb to trunk fat (RLF; > 34%, P < 0.001), hepatic insulin sensitivity (> 40%, P < 0.03), incremental glucose disposal (>50%, P < 0.001) and incremental exogenous glucose storage (>50%, P < 0.05). Furthermore, LIPO displayed reduced incremental glucose oxidation (P < 0.01), increased clamp free fatty acids (P < 0.05) and attenuated insulin-mediated suppression of lipid oxidation (P < 0.05) compared with NONLIPO. In combined study groups, RLF correlated with hepatic insulin sensitivity (r = 0.69), incremental glucose disposal (r = 0.71) and incremental exogenous glucose storage (r = 0.40), all P < 0.01. Disposition index (i.e. first-phase insulin response to intravenous glucose multiplied by incremental glucose disposal) was reduced by 46% (P = 0.05) in LIPO compared with the combined groups of NONLIPO and NAIVE, indicating an impaired adaptation of beta-cell function to insulin resistance in LIPO. CONCLUSION: Our data suggest that normoglycaemic lipodystrophic HIV-infected patients display impaired glucose and lipid metabolism in multiple pathways involving liver, muscle tissue and beta-cell function.",

author = "Haugaard, {Steen B} and Ove Andersen and Flemming Dela and Holst, {Jens Juul} and Heidi Storgaard and Mogens Fenger and Johan Iversen and Sten Madsbad and Haugaard, {Steen B} and Ove Andersen and Flemming Dela and Holst, {Jens Juul} and Heidi Storgaard and Mogens Fenger and Johan Iversen and Sten Madsbad",

note = "Keywords: Adult; Alanine; Antiretroviral Therapy, Highly Active; Blood Glucose; Body Composition; Cholesterol, HDL; Fatty Acids, Nonesterified; Glucagon; Glucose; Glycerol; HIV; HIV-Associated Lipodystrophy Syndrome; Humans; Insulin; Islets of Langerhans; Lactic Acid; Liver; Male; Middle Aged; Muscle, Skeletal; Triglycerides; Tritium",

year = "2005",

language = "English",

volume = "152",

pages = "103--112",

journal = "European Journal of Endocrinology",

issn = "0804-4643",

publisher = "BioScientifica Ltd.",

number = "1",

}

TY - JOUR

T1 - Defective glucose and lipid metabolism in human immunodeficiency virus-infected patients with lipodystrophy involve liver, muscle tissue and pancreatic beta-cells.

AU - Haugaard, Steen B

AU - Andersen, Ove

AU - Dela, Flemming

AU - Holst, Jens Juul

AU - Storgaard, Heidi

AU - Fenger, Mogens

AU - Iversen, Johan

AU - Madsbad, Sten

AU - Haugaard, Steen B

AU - Andersen, Ove

AU - Dela, Flemming

AU - Holst, Jens Juul

AU - Storgaard, Heidi

AU - Fenger, Mogens

AU - Iversen, Johan

AU - Madsbad, Sten

N1 - Keywords: Adult; Alanine; Antiretroviral Therapy, Highly Active; Blood Glucose; Body Composition; Cholesterol, HDL; Fatty Acids, Nonesterified; Glucagon; Glucose; Glycerol; HIV; HIV-Associated Lipodystrophy Syndrome; Humans; Insulin; Islets of Langerhans; Lactic Acid; Liver; Male; Middle Aged; Muscle, Skeletal; Triglycerides; Tritium

PY - 2005

Y1 - 2005

N2 - OBJECTIVES: Lipodystrophy and insulin resistance are prevalent among human immunodeficiency virus (HIV)-infected patients on combined antiretroviral therapy (HAART). Aiming to provide a detailed description of the metabolic adverse effects of HIV-lipodystrophy, we investigated several aspects of glucose metabolism, lipid metabolism and beta-cell function in lipodystrophic HIV-infected patients. METHODS: [3-3H]glucose was applied during euglycaemic hyperinsulinaemic clamps in association with indirect calorimetry in 43 normoglycaemic HIV-infected patients (18 lipodystrophic patients on HAART (LIPO), 18 patients without lipodystrophy on HAART (NONLIPO) and seven patients who were naive to antiretroviral therapy (NAIVE) respectively). beta-cell function was evaluated by an intravenous glucose tolerance test. RESULTS: Compared with NONLIPO and NAIVE separately, LIPO displayed markedly reduced ratio of limb to trunk fat (RLF; > 34%, P < 0.001), hepatic insulin sensitivity (> 40%, P < 0.03), incremental glucose disposal (>50%, P < 0.001) and incremental exogenous glucose storage (>50%, P < 0.05). Furthermore, LIPO displayed reduced incremental glucose oxidation (P < 0.01), increased clamp free fatty acids (P < 0.05) and attenuated insulin-mediated suppression of lipid oxidation (P < 0.05) compared with NONLIPO. In combined study groups, RLF correlated with hepatic insulin sensitivity (r = 0.69), incremental glucose disposal (r = 0.71) and incremental exogenous glucose storage (r = 0.40), all P < 0.01. Disposition index (i.e. first-phase insulin response to intravenous glucose multiplied by incremental glucose disposal) was reduced by 46% (P = 0.05) in LIPO compared with the combined groups of NONLIPO and NAIVE, indicating an impaired adaptation of beta-cell function to insulin resistance in LIPO. CONCLUSION: Our data suggest that normoglycaemic lipodystrophic HIV-infected patients display impaired glucose and lipid metabolism in multiple pathways involving liver, muscle tissue and beta-cell function.

AB - OBJECTIVES: Lipodystrophy and insulin resistance are prevalent among human immunodeficiency virus (HIV)-infected patients on combined antiretroviral therapy (HAART). Aiming to provide a detailed description of the metabolic adverse effects of HIV-lipodystrophy, we investigated several aspects of glucose metabolism, lipid metabolism and beta-cell function in lipodystrophic HIV-infected patients. METHODS: [3-3H]glucose was applied during euglycaemic hyperinsulinaemic clamps in association with indirect calorimetry in 43 normoglycaemic HIV-infected patients (18 lipodystrophic patients on HAART (LIPO), 18 patients without lipodystrophy on HAART (NONLIPO) and seven patients who were naive to antiretroviral therapy (NAIVE) respectively). beta-cell function was evaluated by an intravenous glucose tolerance test. RESULTS: Compared with NONLIPO and NAIVE separately, LIPO displayed markedly reduced ratio of limb to trunk fat (RLF; > 34%, P < 0.001), hepatic insulin sensitivity (> 40%, P < 0.03), incremental glucose disposal (>50%, P < 0.001) and incremental exogenous glucose storage (>50%, P < 0.05). Furthermore, LIPO displayed reduced incremental glucose oxidation (P < 0.01), increased clamp free fatty acids (P < 0.05) and attenuated insulin-mediated suppression of lipid oxidation (P < 0.05) compared with NONLIPO. In combined study groups, RLF correlated with hepatic insulin sensitivity (r = 0.69), incremental glucose disposal (r = 0.71) and incremental exogenous glucose storage (r = 0.40), all P < 0.01. Disposition index (i.e. first-phase insulin response to intravenous glucose multiplied by incremental glucose disposal) was reduced by 46% (P = 0.05) in LIPO compared with the combined groups of NONLIPO and NAIVE, indicating an impaired adaptation of beta-cell function to insulin resistance in LIPO. CONCLUSION: Our data suggest that normoglycaemic lipodystrophic HIV-infected patients display impaired glucose and lipid metabolism in multiple pathways involving liver, muscle tissue and beta-cell function.

M3 - Journal article

SN - 0804-4643

VL - 152

SP - 103

EP - 112

JO - European Journal of Endocrinology

JF - European Journal of Endocrinology

IS - 1

ER -