Transient chylomicronemia preceding the onset of insulin-dependent diabetes in a young girl with no humoral markers of islet autoimmunity

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    Abstract

    Abstract OBJECTIVE: We investigated the possible causes of diabetes in a young child who presented with hyperglycemia associated with severe hypertriglyceridemia (>166 mmol/l), hypercholesterolemia (>38 mmol/l) and fasting chilomicrons. RESULTS: The patient did not have any of the HLA and autoantibody markers typically associated with type 1 diabetes. A glucose clamp failed to demonstrate insulin resistance (peripheral glucose utilization rate (M)=4.3 mg/kg per min) and there was no family history of type 2 diabetes or maturity onset diabetes in youth. Both fasting and stimulated C-peptide levels, including those in response to i.v. glucagon, were below the limit of detection. This is consistent with loss of beta-cell function. The family history did not reveal the existence of relatives with lipid abnormalities, coronary heart disease, and pancreatitis. We did not find any abnormality of plasma apoCII, lipoproteinlipase and hepatic lipase activities. The patients had a epsilon3/epsilon3 apoE genotype and she rapidly cleared an oral fat load after normalization of plasma lipids. CONCLUSIONS: The mild hyperglycemia seems an unlikely explanation for both the severe hypertriglyceridemia and chylomicronemia. A more plausible explanation is transient lipoproteinlipase deficiency. This rare condition, occasionally associated with a high-fat diet, could have caused the rapid and dramatic hypertriglyceridemia observed in this patient, which in turn might have led to the beta-cell destruction by direct lipid toxicity.
    Lingua originaleEnglish
    pagine (da-a)831-836
    Numero di pagine6
    RivistaEUROPEAN JOURNAL OF ENDOCRINOLOGY
    Volume150
    Stato di pubblicazionePublished - 2004

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    Hypertriglyceridemia
    Autoimmunity
    Insulin
    Lipids
    Hyperglycemia
    Type 2 Diabetes Mellitus
    Fasting
    Glucose Clamp Technique
    C-Peptide
    High Fat Diet
    Apolipoproteins E
    Hypercholesterolemia
    Glucagon
    Lipase
    Type 1 Diabetes Mellitus
    Pancreatitis
    Autoantibodies
    Coronary Disease
    Insulin Resistance
    Limit of Detection

    All Science Journal Classification (ASJC) codes

    • Endocrinology

    Cita questo

    @article{ab29d2651b7a4fa38aaa061713b2aa09,
    title = "Transient chylomicronemia preceding the onset of insulin-dependent diabetes in a young girl with no humoral markers of islet autoimmunity",
    abstract = "Abstract OBJECTIVE: We investigated the possible causes of diabetes in a young child who presented with hyperglycemia associated with severe hypertriglyceridemia (>166 mmol/l), hypercholesterolemia (>38 mmol/l) and fasting chilomicrons. RESULTS: The patient did not have any of the HLA and autoantibody markers typically associated with type 1 diabetes. A glucose clamp failed to demonstrate insulin resistance (peripheral glucose utilization rate (M)=4.3 mg/kg per min) and there was no family history of type 2 diabetes or maturity onset diabetes in youth. Both fasting and stimulated C-peptide levels, including those in response to i.v. glucagon, were below the limit of detection. This is consistent with loss of beta-cell function. The family history did not reveal the existence of relatives with lipid abnormalities, coronary heart disease, and pancreatitis. We did not find any abnormality of plasma apoCII, lipoproteinlipase and hepatic lipase activities. The patients had a epsilon3/epsilon3 apoE genotype and she rapidly cleared an oral fat load after normalization of plasma lipids. CONCLUSIONS: The mild hyperglycemia seems an unlikely explanation for both the severe hypertriglyceridemia and chylomicronemia. A more plausible explanation is transient lipoproteinlipase deficiency. This rare condition, occasionally associated with a high-fat diet, could have caused the rapid and dramatic hypertriglyceridemia observed in this patient, which in turn might have led to the beta-cell destruction by direct lipid toxicity.",
    author = "Barbagallo, {Carlo Maria} and Maurizio Averna and Carla Giordano and Cefalu', {Angelo Baldassare} and Manfredi Rizzo and Roberto Citarrella and Alberto Pugliese",
    year = "2004",
    language = "English",
    volume = "150",
    pages = "831--836",
    journal = "EUROPEAN JOURNAL OF ENDOCRINOLOGY",

    }

    TY - JOUR

    T1 - Transient chylomicronemia preceding the onset of insulin-dependent diabetes in a young girl with no humoral markers of islet autoimmunity

    AU - Barbagallo, Carlo Maria

    AU - Averna, Maurizio

    AU - Giordano, Carla

    AU - Cefalu', Angelo Baldassare

    AU - Rizzo, Manfredi

    AU - Citarrella, Roberto

    AU - Pugliese, Alberto

    PY - 2004

    Y1 - 2004

    N2 - Abstract OBJECTIVE: We investigated the possible causes of diabetes in a young child who presented with hyperglycemia associated with severe hypertriglyceridemia (>166 mmol/l), hypercholesterolemia (>38 mmol/l) and fasting chilomicrons. RESULTS: The patient did not have any of the HLA and autoantibody markers typically associated with type 1 diabetes. A glucose clamp failed to demonstrate insulin resistance (peripheral glucose utilization rate (M)=4.3 mg/kg per min) and there was no family history of type 2 diabetes or maturity onset diabetes in youth. Both fasting and stimulated C-peptide levels, including those in response to i.v. glucagon, were below the limit of detection. This is consistent with loss of beta-cell function. The family history did not reveal the existence of relatives with lipid abnormalities, coronary heart disease, and pancreatitis. We did not find any abnormality of plasma apoCII, lipoproteinlipase and hepatic lipase activities. The patients had a epsilon3/epsilon3 apoE genotype and she rapidly cleared an oral fat load after normalization of plasma lipids. CONCLUSIONS: The mild hyperglycemia seems an unlikely explanation for both the severe hypertriglyceridemia and chylomicronemia. A more plausible explanation is transient lipoproteinlipase deficiency. This rare condition, occasionally associated with a high-fat diet, could have caused the rapid and dramatic hypertriglyceridemia observed in this patient, which in turn might have led to the beta-cell destruction by direct lipid toxicity.

    AB - Abstract OBJECTIVE: We investigated the possible causes of diabetes in a young child who presented with hyperglycemia associated with severe hypertriglyceridemia (>166 mmol/l), hypercholesterolemia (>38 mmol/l) and fasting chilomicrons. RESULTS: The patient did not have any of the HLA and autoantibody markers typically associated with type 1 diabetes. A glucose clamp failed to demonstrate insulin resistance (peripheral glucose utilization rate (M)=4.3 mg/kg per min) and there was no family history of type 2 diabetes or maturity onset diabetes in youth. Both fasting and stimulated C-peptide levels, including those in response to i.v. glucagon, were below the limit of detection. This is consistent with loss of beta-cell function. The family history did not reveal the existence of relatives with lipid abnormalities, coronary heart disease, and pancreatitis. We did not find any abnormality of plasma apoCII, lipoproteinlipase and hepatic lipase activities. The patients had a epsilon3/epsilon3 apoE genotype and she rapidly cleared an oral fat load after normalization of plasma lipids. CONCLUSIONS: The mild hyperglycemia seems an unlikely explanation for both the severe hypertriglyceridemia and chylomicronemia. A more plausible explanation is transient lipoproteinlipase deficiency. This rare condition, occasionally associated with a high-fat diet, could have caused the rapid and dramatic hypertriglyceridemia observed in this patient, which in turn might have led to the beta-cell destruction by direct lipid toxicity.

    UR - http://hdl.handle.net/10447/9655

    M3 - Article

    VL - 150

    SP - 831

    EP - 836

    JO - EUROPEAN JOURNAL OF ENDOCRINOLOGY

    JF - EUROPEAN JOURNAL OF ENDOCRINOLOGY

    ER -