A case of hyperchylomicronemia associated with GPIHBP1 autoantibodies and fluctuating thyroid autoimmune disease

Nozue, Tsuyoshi; Tada, Hayato; Murakami, Masami; Michishita, Ichiro

doi:10.1016/j.jacl.2022.10.005

Cited by 4 publications

(1 citation statement)

References 20 publications

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“…The patient was finally treated with rituximab and methylprednisolone, which resulted in the disappearance of GPIHBP1 autoantibodies and normalization of plasma TG levels 44 . To date, cases with autoimmune diseases, such as SLE 45 , 46 , 47 , antiphospholipid syndrome 46 and Graves' disease 46 , 48 , have been reported, and they were successfully treated with immunosuppressive treatments with prednisolone, rituximab and mycophenolate mofetil.…”

Section: Autoantibodies In Severe Hypertriglyceridemiamentioning

confidence: 99%

Role of glycosylphosphatidylinositol‐anchored high‐density lipoprotein binding protein 1 in hypertriglyceridemia and diabetes

Kurooka

Eguchi

Wada

2023

J of Diabetes Invest

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In diabetes, the impairment of insulin secretion and insulin resistance contribute to hypertriglyceridemia, as the enzymatic activity of lipoprotein lipase (LPL) depends on insulin action. The transport of LPL to endothelial cells and its enzymatic activity are maintained by the formation of lipolytic complex depending on the multiple positive (glycosylphosphatidylinositol‐anchored high‐density lipoprotein binding protein 1 [GPIHBP1], apolipoprotein C‐II [APOC2], APOA5, heparan sulfate proteoglycan [HSPG], lipase maturation factor 1 [LFM1] and sel‐1 suppressor of lin‐12‐like [SEL1L]) and negative regulators (APOC1, APOC3, angiopoietin‐like proteins [ANGPTL]3, ANGPTL4 and ANGPTL8). Among the regulators, GPIHBP1 is a crucial molecule for the translocation of LPL from parenchymal cells to the luminal surface of capillary endothelial cells, and maintenance of lipolytic activity; that is, hydrolyzation of triglyceride into free fatty acids and monoglyceride, and conversion from chylomicron to chylomicron remnant in the exogenous pathway and from very low‐density lipoprotein to low‐density lipoprotein in the endogenous pathway. The null mutation of GPIHBP1 causes severe hypertriglyceridemia and pancreatitis, and GPIGBP1 autoantibody syndrome also causes severe hypertriglyceridemia and recurrent episodes of acute pancreatitis. In patients with type 2 diabetes, the elevated serum triglyceride levels negatively correlate with circulating LPL levels, and positively with circulating APOC1, APOC3, ANGPTL3, ANGPTL4 and ANGPTL8 levels. In contrast, circulating GPIHBP1 levels are not altered in type 2 diabetes patients with higher serum triglyceride levels, whereas they are elevated in type 2 diabetes patients with diabetic retinopathy and nephropathy. The circulating regulators of lipolytic complex might be new biomarkers for lipid and glucose metabolism, and diabetic vascular complications.

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