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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Secondary hyperlipidaemia is common and occurs frequently in disorders such as obesity, alcoholism, diabetes mellitus, hypothyroidism, liver and renal diseases and as a side-effect of drug therapy, particularly for hypertension. Its management may be important to prevent complications such as coronary heart disease and acute pancreatitis. Its study provides many fascinating insights into lipoprotein pathophysiology.
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PMID:Secondary hyperlipidaemia. 210 Jun 85

Secondary hyperlipidemia is a common laboratory finding in children with nephrotic syndrome, diabetes mellitus, and hypothyroidism. However, clinical signs of hyperlipidemia are extremely rare in childhood. We report on an 11-year-old girl who presented with a disseminated yellow papulomatous rash on the lower limbs and yellow skin creases on the palms of her hands. Blood tests yielded an opaque serum with a triglyceride concentration of 820 mg/dL and cholesterol of 1050 mg/dL. Skin biopsy of one of the papules confirmed the diagnosis of xanthomas. Additional examinations revealed clinical (weight gain, diminished growth rate) and biochemical primary hypothyroidism (free T4: 0.4 ng/L [normal 8-22 ng/L]; thyroid-stimulating hormone: >200 mU/L) as a consequence of Hashimoto thyroiditis (thyroid peroxidase and thyroglobulin: 4400 U/mL and >2000 U/mL, respectively; normal <60 U/mL). The patient was started on L-thyroxine, which led to a gradual decline of cholesterol and triglycerides to normal concentrations and a complete remission from the xanthomatous rash. For the first time, this case depicts disseminated xanthomas of the skin as the presenting complaint of severe hypothyroidism. hyperlipidemia, hypothyroidism, xanthoma.
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PMID:Unmasking of childhood hypothyroidism by disseminated xanthomas. 1169 80

Secondary hyperlipidemia is a major cardiovascular risk factor in individuals with type 2 diabetes. Increased hepatic production of apolipoprotein B (apoB)-containing lipoproteins contributes to the elevated plasma levels, but the mechanism is poorly understood. Recent results have established that microsomal triglyceride transfer protein (MTP) is rate limiting for the assembly and secretion of apoB-containing lipoproteins. To better understand the mechanism of type 2 diabetes-associated hyperlipidemia, we quantified hepatic MTP mRNA levels, hepatic microsomal triglyceride transfer activity, and in vivo triglyceride secretion from the liver in two diabetic mouse models. Obese diabetic (ob/ob) mice had 45% higher (P = 0.006) hepatic MTP mRNA levels, 54% higher (P < 0.0001) microsomal triglyceride transfer activity, and 70% higher (P < 0.0001) in vivo triglyceride secretion rates compared with ob/+ control mice. In contrast, in lean streptozotocin-treated diabetic mice, hepatic MTP mRNA levels were unchanged, whereas microsomal triglyceride transfer activity and in vivo triglyceride secretion rates were marginally decreased. These studies suggest that obesity-induced type 2 diabetes in mice confers increases in hepatic MTP expression and secretion of triglyceride-rich lipoproteins. High blood glucose and altered hepatic expression of sterol regulatory element binding protein genes play a minor role in this diabetic response.
Diabetes 2002 Apr
PMID:Hepatic expression of microsomal triglyceride transfer protein and in vivo secretion of triglyceride-rich lipoproteins are increased in obese diabetic mice. 1191 50

The disturbance of lipid metabolism is seen in some inherited diseases and also in patients with some kinds of underlying diseases. The presence of its disturbance can be detected by measuring the concentrations of cholesterol and triglyceride in serum. Although hyperlipidemia or hypolipidemia is the result of abnormal lipid metabolism, hyperlipidemia is of more concern to physicians because of the close association with atherosclerosis. Responsible genes for some primary (or hereditary) hyperlipidemic diseases have been confirmed as follows; LPL or apo C-II for primary chylomicronemia, LDL receptor for familial hypercholesterolemia and apo B-100 for familial defective apo B-100. However, the responsible gene remains controversial for familial combined hyperlipidemia, though AI/CIII/AIV cluster is one of the possible candidate genes. Secondary hyperlipidemia is caused by various diseases such as diabetes mellitus, renal diseases and cholestasis. This type of hyperlipidemia is improved by therapy for the underlying diseases. To date, the mechanism of lipid metabolism has been defined in a molecular basis. In fact, sterol regulatory element-binding protein (SREBP), peroxisome proliferator-activated receptor (PPAR) and ATP-binding cassette transporter subfamily A, member 1(ABCA1) were recently identified and it was demonstrated that these regulate lipid metabolism.
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PMID:[Disturbance of lipid metabolism]. 1198 47

Secondary hyperlipidemia is common and occurs frequently in patients with endocrine disease such as hy- pothyroidism, Cushing's syndrome, and acromegaly, metabolic disease such as diabetes mellitus, renal dis- ease such as nephrotic syndrome and chronic renal failure, liver disease such as obstructive liver disease, and as a side-effect of glucocorticoids and estrogens. The underlying cause of high serum lipid levels will often be missed if it is not actively sought. We describe. the causes and abnormal lipid laboratory values of sec- ondary hyperlipidemia in endocrine disease patients such as those with hypothyroidism, Cushing's syndrome, and acromegaly. Hypothyroidism is associated with elevated serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), and normal or elevated high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG), respectively. The lipid abnormalities are due to the reductions in hepatic LDL receptor function and hepatic TG lipase (HTGL) activity. Cushing's syndrome is associated with elevated serum TC, LDL-C, and TG and elevated or normal HDL-C. The lipid abnormalities are due to the glucocorticoid- induced increase in very low-density lipoprotein (VLDL) and elevation in lipoprotein lipase (LPL) activity. Acromegaly is associated with normal serum TC, reduced LDL-C and HDL-C, and elevated TG. The lipid abnormalities are due to the growth hormone-induced reductions in LPL and HTGL activity and increase in hepatic LDL receptors. When we examine hyperlipidemic patients, it is important to diagnose the true name of the disease, usually in consideration of the possibility of the cause of secondary hyperlipidemia. [Review].
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PMID:[Causes and Abnormal Lipid Laboratory Values of Secondary Hyperlipidemia: Endocrine Disease]. 3069 60