Influence of Prolonged Fasting on the Serum and Hepatic Lipid Levels in Immature and Mature Rats

1993 ◽  
Vol 57 (3) ◽  
pp. 493-494
Author(s):  
Yukio Furuichi ◽  
Takao Takahashi
Author(s):  
Elise F. Hoek-van den Hil ◽  
Jaap Keijer ◽  
Annelies Bunschoten ◽  
Jacques J. M. Vervoort ◽  
Barbora Stankova ◽  
...  

Animals ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 1098 ◽  
Author(s):  
Yu Niu ◽  
Jintian He ◽  
Yongwei Zhao ◽  
Mingming Shen ◽  
Lili Zhang ◽  
...  

The possible causes of intrauterine growth retardation (IUGR) might stem from placental insufficiency, maternal malnutrition, inflammation in utero, and other causes. IUGR has had an adverse influence on human health and animal production. Forty weaned piglets with normal birth weights (NBWs) or IUGR were randomly divided into four treatments groups: NBW, NC (NBW with curcumin supplementation), IUGR, and IC (IUGR with curcumin supplementation) from 26 to 50 d. Levels of cytokines, glucose, and lipid metabolism were evaluated. IUGR piglets showed slow growth during the experiment. Piglets with IUGR showed higher levels of serum pro-inflammatory cytokines, insulin resistance, and hepatic lipid accumulation. Curcumin supplementation reduced the production of serum pro-inflammatory cytokines, attenuated insulin resistance and hepatic triglyceride, and enhanced the hepatic glycogen concentrations and lipase activities of IUGR piglets. The hepatic mRNA expressions of the insulin-signaling pathway and lipogenic pathway were influenced by IUGR and were positively attenuated by diets supplemented with curcumin. In conclusion, IUGR caused slow growth, insulin resistance, and increased hepatic lipid levels. Diets supplemented with curcumin improved growth, attenuated insulin resistance, and reduced lipid levels in the liver by regulating the hepatic gene expressions of the related signaling pathway in IUGR piglets.


2012 ◽  
Vol 53 (4) ◽  
pp. 686-695 ◽  
Author(s):  
Shunxing Rong ◽  
Qiang Cao ◽  
Mingxia Liu ◽  
Jeongmin Seo ◽  
Lin Jia ◽  
...  
Keyword(s):  

1988 ◽  
Vol 254 (1) ◽  
pp. 245-254 ◽  
Author(s):  
M E Hahn ◽  
T A Gasiewicz ◽  
P Linko ◽  
J A Goldstein

The role of the Ah locus in hexachlorobenzene (HCB)-induced porphyria and the possible involvement of P-450 cytochromes P(1)450 and P(3)450 in the pathogenesis of this disease were investigated in two congenic strains of C57BL/6J mice that differ only at this locus. Female B6-Ahb mice (Ah receptor: approximately 30-70 fmol/mg of cytosolic protein) and B6-Ahd mice (Ah receptor: undetectable) were pretreated with iron (500 mg/kg) and then fed a diet containing 0 or 200 p.p.m. of HCB for up to 17 weeks. Mice from the two strains consumed similar amounts of HCB. Urinary excretion of porphyrins was increased after 7 weeks of HCB treatment in B6-Ahb mice, and after 15 weeks was over 200 times greater than that of mice given iron only. In B6-Ahd mice, porphyrin excretion did not begin to increase until after 13 weeks, and after 15 weeks was only six times greater than that of controls. Similar differences were seen in the 15-week hepatic porphyrin concentrations (B6-Ahb: 1110 +/- 393; B6-Ahd: 17.6 +/- 14.5; controls: approximately 0.20 nmol/g). Uroporphyrinogen decarboxylase (EC 4.1.1.37) activity was diminished by 70 and 20% in B6-Ahb B6-Ahd mice respectively after 15 weeks of treatment with HCB. Cytochromes P(1)450 and P(3)450 were measured in hepatic microsomes (microsomal fractions) by radioimmunoassay and immunoblotting, using antisera raised against the orthologous rat isoenzymes P450c and P450d. HCB induced small amounts of a protein recognized by anti-P450c (P(1)450) in B6-Ahd mice, but not in B6-Ahd mice. Relatively large amounts of a protein recognized by anti-P450d (P(3)450) were induced in both strains, but to a somewhat greater extent in the B6-Ahb mice. The hepatic accumulation of HCB at 15 weeks was greater in B6-Ahb than in B6-Ahd mice, in association with elevated hepatic lipid levels in the former strain. The results of this experiment indicate that the Ah locus influences the susceptibility of C57BL/6J mice to HCB-induced porphyria and are consistent with the suggestion that the sustained induction of P(3)450 and/or P(1)450 may be a causative factor in the development of this disease.


PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e51588 ◽  
Author(s):  
Elise F. Hoek-van den Hil ◽  
Jaap Keijer ◽  
Annelies Bunschoten ◽  
Jacques J. M. Vervoort ◽  
Barbora Stankova ◽  
...  

2005 ◽  
Vol 25 (9) ◽  
pp. 869-876 ◽  
Author(s):  
Sung-Hyeon Lee ◽  
Hong-Ju Park ◽  
So-Young Cho ◽  
Hyun-Jin Jung ◽  
Soo-Mook Cho ◽  
...  

Lipids ◽  
1971 ◽  
Vol 6 (5) ◽  
pp. 332-340 ◽  
Author(s):  
Shmuel Kerpel ◽  
Bernard Rubenstein ◽  
David Rubinstein

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