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Prenatal nicotine exposure (PNE) induces skeletal growth retardation and dyslipidemia in offspring displaying intrauterine growth retardation (IUGR). Cholesterol accumulation resulting from cholesterol efflux dysfunction may reduce the quality of articular cartilage through fetal programming. This study evaluated the quality of articular cartilage of female adult offspring fed a high-fat diet and explored the mechanisms using a rat IUGR model established by the administration of 2.0 mg/kg/d of subcutaneous nicotine from gestational days 11–20. The results demonstrated an increased OARSI (Osteoarthritis Research Society International) score and total cholesterol content, decreased serum corticosterone, and increased IGF1 and dyslipidemia with catch-up growth in PNE adult offspring. Cartilage matrix, IGF1 and cholesterol efflux pathway expression were reduced in PNE fetuses and adult offspring. Therefore, PNE induced poor articular cartilage quality in female adult offspring fed a high-fat diet via a dual programming mechanism. [ABSTRACT FROM AUTHOR]

Familial hypercholesterolemia (FH MIM# 143890 ) is one of the most common autosomal inherited diseases. FH is characterized by elevated plasma levels of total cholesterol and low-density lipoprotein-cholesterol. Mutation in the LDLR gene, which encodes the LDL receptor protein, is responsible for most of the morbidity of FH. The incidence of heterozygous FH is about 1/500, whereas the incidence of homozygous FH is only 1/1,000,000 in Caucasian population. In this study, we report a homozygous LDLR mutation (c.298G > A) in a familial hypercholesterolemia patient, who exhibited intracranial cholesterol deposition, which is a rare addition to the common FH phenotypes. The proband's consanguineous parents have the same heterozygous mutation with elevated concentrations of LDL-C but no xanthoma. [ABSTRACT FROM AUTHOR]

• Broiler chicken diet was supplemented with the fermentation concentrate of Hericium caput-medusae (Bull.:Fr.) Pers. (HFC) at 4 concentrations (0, 0.6, 1.2, and 1.8%). • Supplementation with HFC increased serum high-density lipoprotein cholesterol concentration in broiler chickens. • Supplementation with HFC decreased the cholesterol content in meat and liver of broiler chickens. • Supplementation with HFC may be a potential way to produce the low-cholesterol chicken demanded by consumers. The fermentation concentrate of Hericium caput-medusae (Bull.:Fr.) Pers. (HFC) is a liquid fermentation product of fungi. The purpose of this study was to investigate the effects of dietary supplementation with HFC on cholesterol deposition in the liver and meat, as well as the production of short chain fatty acids (SCFA) in the cecum of broiler chickens. A total of 480 male broiler chickens (1- d -old, initial body weight of 38.8 ± 0.9 g) were randomly assigned to 4 dietary treatments with 6 cages/treatment and 20 broiler chickens/cage. The broiler chickens in the 4 treatments received diets supplemented with 0, 0.6, 1.2, and 1.8% of HFC during the 42-d feeding experiment. The results showed that the serum total cholesterol, triglyceride, and low-density lipoprotein cholesterol concentrations decreased linearly (P < 0.05) and quadratically (P < 0.05) as the dietary HFC supplementation increased. The cholesterol contents in the liver, thigh, and breast muscles of broiler chickens decreased linearly (P < 0.05) and quadratically (P < 0.05) with increasing HPC supplementation. The serum high-density lipoprotein cholesterol concentration and excreta bile acid content increased linearly (P < 0.05) and quadratically (P < 0.05) with the increase of dietary HFC supplementation. The gene expression of 3‑hydroxy‑3-methyl-glutaryl-coenzyme A reductase (HMGR) in the liver of broiler chickens decreased linearly (P < 0.05) and quadratically (P < 0.05) as the dietary HFC supplementation increased. The contents of propionic acid and butyric acid increased linearly (P < 0.05) and quadratically (P < 0.05) as the dietary supplementation of HFC increased. The cholesterol-lowering effects of this treatment might be attributed to the decrease in the gene expression of HMGR in the liver, the increase in SCFA production in the cecum, and the increase in bile acids in the excreta by HFC. Therefore, supplementation of HFC in the diet of broiler chickens may be a means of producing the low-cholesterol chicken demanded by consumers. [ABSTRACT FROM AUTHOR]