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Results for “Lipid Metabolism Disorders”

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At least 19 recordsLinked to original sources
PubMedDate not supplied

[Lipid metabolic disorders and lipid peroxidation in patients with the nephrotic syndrome].

Lipid metabolism was studied in 161 patients with renal diseases, 62 of them had nephrotic syndrome (NS). The measurements were made of cholesterol, triglycerides, dienic conjugates, B2-microglobulins in urine and blood, functional and morphological parameters, red cell resistance to peroxide hemolysis. It was found that NS patients, especially those with additional renal failure, displayed high-intensity lipoperoxidation (LPO). LPO intensity proved unrelated to NS etiology. NS-associated hyperlipidemia gives rise to multifunctional biomembrane instability responsible for antioxidant disorders.

Adult↗
PubMedDate not supplied

The cornea and disorders of lipid metabolism.

Disorders of lipid metabolism, either hyperlipidemia or hypolipidemia, are associated with the formation of corneal opacities. Corneal arcus, the most commonly encountered peripheral corneal opacity, is frequently associated with abnormal serum lipid levels, but may occur without any predisposing factors. Reports also have linked corneal arcus with alcoholism, diabetes mellitus and atherosclerotic heart disease. Unilateral arcus is a rare entity that is associated with carotid artery disease or ocular hypotony. Diffuse corneal opacities associated with hypolipidemic disorders such as LCAT deficiency, fish eye disease and Tangier disease, may be the initial manifestation of these disorders and puts the ophthalmologist in a position to make an early diagnosis. Corneal arcus, along with a central corneal opacity, is seen in Schnyder's crystalline stromal distrophy. The association of the disorder with a dyslipidemia remains controversial. A review of lipid metabolism, corneal arcus and several disorders of lipid metabolism that affect the cornea are presented.

Alcoholism↗
PubMed2026

Excess iodine induces lipid metabolic disorders by the gut microbiota SCFAs/H2S-p-AMPKα/PPARγ/SREBP-1c pathway in female rats.

With the development of living standards, the problem of excess iodine has long been overlooked. This study aimed to investigate the detrimental effects of long-term excess iodine exposure on lipid metabolism in female Sprague-Dawley rats from the gut-liver axis perspective, and to elucidate the underlying molecular mechanisms by which the gut microbiota and its metabolites mediate iodine-induced lipid metabolic disorders. The results indicated that abnormal iodine nutrition has a negative effect on the health of rats. Specifically, excess iodine not only causes thyroid disorders but also leads to liver lipid metabolism disorders, including elevated serum and hepatic total cholesterol/triglyceride levels and lipid accumulation in the liver. Further investigation revealed that excess iodine causes liver lipid metabolism disorders by altering the gut microbiota, which resulted in an increase in the relative abundance of Desulfovibrio and Lachnospiraceae NK4A136_group, and a decrease in the relative abundance of Akkermansia and Blautia in excess iodine groups. A decrease in the relative abundance of Blautia and an increase in Lachnospiraceae NK4A136_group were strongly correlated with reductions in short-chain fatty acids (acetic, propionic, and valeric acids), whereas an increase in Desulfovibrio was strongly correlated with an increase in H2S. Additionally, acetic acid was negatively correlated with H2S in serum and liver. Excess iodine reduced hepatic p-AMPKα expression while upregulating key regulators of lipid metabolism, including SREBP-1c, PPARγ and ACC1. These changes may represent one of the key mechanisms by which excess iodine induces lipid metabolism disorders through the microbiota-metabolite axis. Overall, these findings suggest that excess iodine influences lipid metabolism through the gut-liver axis. The results of this study provide scientific references and guidance for the appropriate intake of iodine and offer novel insights for early nutritional interventions targeting lipid metabolism disorders.

Journal Article↗
PubMed2006

[Effect of selenium supplement on the disordered lipid metabolism induced by the overdose of iodine in mice].

OBJECTIVE: To explore the effect of selenium supplement on the disordered lipid metabolism induced by the overdose of iodine in mice. METHODS: The 80 Balb/c mice were randomly divided into eight groups, the normal control group, the high iodine group (drunk the water containing iodine 3000 microg/L) and six selenium groups (drunk the water containing iodine 3000 microg/L and selenium 0.1, 0.2, 0.3, 0.4, 0.5, 0.75 mg/L). The total cholesterol and triglyceride in serum and liver were determined. RESULTS: The total cholesterol in serum, the total cholesterol and triglyceride in liver of high-iodine group increased significantly compared with normal control group. There is no difference between normal control group and the group drunk the water contained 0.2 mg/L selenium. CONCLUSION: It suggests that it is an effective intervention dosage to drunk water containing 0.2 mg/L selenium.

Animals↗
PubMed2003

[Molecular mechanism of wendan tang in prevention of lipid metabolism disorder in adult rats].

OBJECTIVE: To elucidate the molecular mechanism of Wendan Tang in prevention of lipid metabolism disorder in adult rats. METHOD: On the basis of hyperlipidemia rat models, triglycerides (TG), total cholesterol (TC) in serum, activities of lipase (LA), lipoprotein lipase (LPL), hepatic lipase (HL) in liver, parts of hemogram and hepatic LDLR mRNA levels were investigated 21 days after the feeding of atherogenic diet. RESULT: Wendan Tang significantly reduced the serum TG, TC and increased the activity of LPL and LA, but caused no chang in HL. The result of RT-PCR test showed that high fat and high cholesterol feeding could significantly induce the reduction of LDLR mRNA levels, while Wendan Tang could increase hepatic LDLR density. CONCLUSION: Wendan Tang can prevent disorder of lipid metabolism by regulating TC, TG, LDL-c through upregaulation of LDLR transcription level and improving antioxidant ability.

Animals↗
PubMedDate not supplied

[The immunomodulating and antioxidant action of beta-carotene and essentiale in a lipid metabolic disorder].

Excessive supply of lipids to the organism of rats causes increase in lipid peroxidation, reduction of red cell energy status, the appearance in them of immunosuppressive properties, and inhibition of immunological reactivity. Administration of beta-carotene and essential corrects the biochemical status and immunological reactivity of the organism in alimentary lipid loading. beta-Carotene cancels the immunosuppressive properties of light red blood cells, whereas essential induces the appearance of immunostimulating properties in the heavy cells.

Adjuvants, Immunologic↗