scholarly journals A decrease in vascular resistance in the sinusoid by elimination of fat deposition in the hepatic cell in the choline deficient diet induced cirrhosis of the rat liver.

Kanzo ◽  
1976 ◽  
Vol 17 (2) ◽  
pp. 92-101
Author(s):  
Yuro SHIBAYAMA ◽  
Katsuji NAKATA
Keyword(s):  
Vascular Resistance ◽  
Rat Liver ◽  
Hepatic Cell ◽  
Fat Deposition ◽  
Deficient Diet

scholarly journals Portal hypertensive response to kinin

2009 ◽  
Vol 81 (3) ◽  
pp. 431-442 ◽  
Author(s):  
Maria Kouyoumdjian ◽  
Marcia R. Nagaoka ◽  
Mauricio R. Loureiro-Silva ◽  
Durval R. Borges
Keyword(s):  
Vascular Resistance ◽  
Rat Liver ◽  
Liver Perfusion ◽  
Stellate Cells ◽  
Kinin System ◽  
Rat Liver Perfusion ◽  
Isolated Liver Cells ◽  
B2 Receptors ◽  
Intrahepatic Vascular Resistance

Portal hypertension is the most common complication of chronic liver diseases, such as cirrhosis. The increased intrahepatic vascular resistance seen in hepatic disease is due to changes in cellular architecture and active contraction of stellate cells. In this article, we review the historical aspects of the kallikrein-kinin system, the role of bradykinin in the development of disease, and our main findings regarding the role of this nonapeptide in normal and experimentalmodels of hepatic injury using the isolated rat liver perfusion model (mono and bivascular) and isolated liver cells. We demonstrated that: 1) the increase in intrahepatic vascular resistance induced by bradykinin is mediated by B2 receptors, involving sinusoidal endothelial and stellate cells, and is preserved in the presence of inflammation, fibrosis, and cirrhosis; 2) the hepatic arterial hypertensive response to bradykinin is calcium-independent and mediated by eicosanoids; 3) bradykinin does not have vasodilating effect on the pre-constricted perfused rat liver; and, 4) after exertion of its hypertensive effect, bradykinin is degraded by angiotensin converting enzyme. In conclusion, the hypertensive response to BK is mediated by the B2 receptor in normal and pathological situations. The B1 receptor is expressed more strongly in regenerating and cirrhotic livers, and its role is currently under investigation.

Effect of phenobarbital on the development of fatty livers In choline-deficient rats

1970 ◽  
Vol 48 (11) ◽  
pp. 1284-1285 ◽  
Author(s):  
A. Chalvardjian
Keyword(s):  
Hepatic Cell ◽  
Choline Deficiency ◽  
Deficient Diet ◽  
Fatty Livers ◽  
Phenobarbital Administration ◽  
Phospholipid Pool

The increase in hepatic phospholipid pool induced by phenobarbital did not affect the hepatic accumulation of fat produced by feeding rats a choline-deficient diet for 4 days. This lack of effect suggests that phenobarbital administration does not increase the choline requirement of rats, and/or that phenobarbital and choline deficiency act on different loci within the hepatic cell independently of each other.

A New Method for Measuring the Speed of Sound in Rat Liver ex Vivo Using an Ultrasound System: Correlation of Sound Speed with Fat Deposition

2014 ◽  
Vol 40 (10) ◽  
pp. 2499-2507 ◽  
Author(s):  
Hideki Kumagai ◽  
Koji Yokoyama ◽  
Kimito Katsuyama ◽  
Shoji Hara ◽  
Hiroaki Yamamoto ◽  
...  
Keyword(s):  
Rat Liver ◽  
Speed Of Sound ◽  
Sound Speed ◽  
Ex Vivo ◽  
Fat Deposition ◽  
New Method ◽  
Ultrasound System

scholarly journals Vitamin B12 deficiency results in the abnormal regulation of serine dehydratase and tyrosine aminotransferase activities correlated with impairment of the adenylyl cyclase system in rat liver

2008 ◽  
Vol 99 (3) ◽  
pp. 503-510 ◽  
Author(s):  
Shuhei Ebara ◽  
Motoyuki Nakao ◽  
Mayuko Tomoda ◽  
Ryoichi Yamaji ◽  
Fumio Watanabe ◽  
...  
Keyword(s):  
Adenylyl Cyclase ◽  
Rat Liver ◽  
Vitamin B12 Deficiency ◽  
Tyrosine Aminotransferase ◽  
Vitamin B ◽  
Deficient Diet ◽  
Adenylyl Cyclase System ◽  
Serine Dehydratase ◽  
B12 Deficiency ◽  
Induced Changes

The aim of the present study was to elucidate the mechanism of the vitamin B12 deficiency-induced changes of the serine dehydratase (SDH) and tyrosine aminotransferase (TAT) activities in the rat liver. When rats were maintained on a vitamin B12-deficient diet, the activities of these two enzymes in the liver were significantly reduced compared with those in the B12-sufficient control rats (SDH 2·8 (sd 0·56) v. 17·5 (sd 6·22) nmol/mg protein per min (n 5); P < 0·05) (TAT 25·2 (sd 5·22) v. 41·3 (sd 8·11) nmol/mg protein per min (n 5); P < 0·05). In the B12-deficient rats, the level of SDH induction in response to the administration of glucagon and dexamethasone was significantly lower than in the B12-sufficient controls. Dexamethasone induced a significant increase in TAT activity in the primary culture of the hepatocytes prepared from the deficient rats, as well as in the cells from the control rats. However, a further increase in TAT activity was not observed in the hepatocytes from the deficient rats, in contrast to the cells from the controls, when glucagon was added simultaneously with dexamethasone. The glucagon-stimulated production of cAMP was significantly reduced in the hepatocytes from the deficient rats relative to the cells from the control rats. Furthermore, the glucagon-stimulated adenylyl cyclase activity in the liver was significantly lower in the deficient rats than in the controls. These results suggest that vitamin B12 deficiency results in decreases in SDH and TAT activities correlated with the impairment of the glucagon signal transduction through the activation of the adenylyl cyclase system in the liver.

scholarly journals Magnesium and calcium deficiencies additively increase zinc concentrations and metallothionein expression in the rat liver

2012 ◽  
Vol 109 (3) ◽  
pp. 425-432 ◽  
Author(s):  
Megumi Kotani ◽  
Ki Hyun Kim ◽  
Natsumi Ishizaki ◽  
Masayuki Funaba ◽  
Tohru Matsui
Keyword(s):  
Rat Liver ◽  
Control Diet ◽  
Mrna Level ◽  
Male Rats ◽  
Mrna Levels ◽  
Deficient Diet ◽  
Mg Deficiency ◽  
Ca Deficiency ◽  
Zn Concentration ◽  
Dietary Treatments

Mg deficiency increases the concentration of Zn in the liver. We investigated the effect of Mg deficiency on the expression of Zn-regulating factors such as Zn transporters and metallothionein (MT) in the rat liver. Because Ca deficiency alleviates some of the effects of Mg deficiency, we also investigated the interactions associated with Ca and Mg deficiencies. Growing male rats were given a control diet, a Mg-deficient diet, a Ca-deficient diet and a Mg- and Ca-deficient diet for 3 weeks. Mg and Ca deficiencies additively increased the mRNA levels of MT-1 and MT-2, the MT protein concentration and the concentration of Zn in the liver. The hepatic mRNA level of Zip14 increased with Mg deficiency but not with Ca deficiency. The dietary treatments did not affect the mRNA levels of other Zn transporters such as Zip1, Zip5, ZnT1, ZnT5 and ZnT6 in the liver. Ca deficiency was found to decrease the amount of femoral Zn and increase serum Zn concentration. This did not occur in the case of Mg deficiency. These results suggest that Mg deficiency enhances hepatic Zn uptake by the up-regulation of Zip14 expression and increases hepatic Zn concentration, leading to the enhancement of MT expression. Ca deficiency causes a transfer of Zn from the bone to the liver, which increases hepatic Zn concentration and, in turn, up-regulates the expression of MT. Because Mg and Ca deficiencies increase hepatic Zn concentration and increase MT expression by different mechanisms, their effects are additive.

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