DYNAMICS OF HEPATIC GLYCOGEN: OESTROGEN AND PREGNANCY

1972 ◽  
Vol 71 (2) ◽  
pp. 385-392 ◽  
Author(s):  
P. K. Paul

ABSTRACT The effects of oestradiol (0.5 μ/rat/day) given for a variable period on rat liver were investigated, and the results were compared with those of untreated pregnant rats at different stages of pregnancy. The part played by the adrenal under these conditions was also investigated. Oestrogen treatment for 14 and 21 days in intact rats reduced the liver glycogen. A corresponding reduction in food intake was noted during these days. However, a rebound rise in liver glycogen occurred after 28 days of oestrogen administration. In contrast, the ovariectomized animals did not show any change in liver glycogen following steroid treatment. During pregnancy the total liver glycogen increased after the first week, but returned to the normal level on day twenty one. The adrenal and serum cholesterol levels in oestrogen treated and pregnant rats remained low except for an increase in serum cholesterol on day 21 of gestation and 7 days after oestrogen treatment. The study suggests that continued oestrogen treatment of non-pregnant rats probably maintains some endogenous factor(s) (progesterone) for about 21 days, which antagonizes the effect of oestrogen administration on hepatic glycogen deposition. The implications of liver glycogen changes during pregnancy in relation to progesterone levels and dietary intake are discussed.

1959 ◽  
Vol 196 (3) ◽  
pp. 603-606 ◽  
Author(s):  
Jean Christophe ◽  
Jean Mayer

Oral treatment with carbutamide (BZ-55) for 7 weeks (2.5 gm/kg of ground chow) left the food intake and rate of weight gain of obese-hyperglycemic mice and lean littermates unmodified as compared with untreated controls. Obese-hyperglycemic animals, after 49 days of treatment showed the usual distribution and rate of biosynthesis of fatty acids and cholesterol in the liver and carcass. Liver hypertrophy, marked increase in serum cholesterol levels and lack of improvement of the ‘diabetes’ were also observed in these animals. Lean littermates similarly treated showed no modification in the distribution of fatty acids and cholesterol and in the biosynthesis of fatty acids in the liver and carcass. An increase in hepatic cholesterologenesis, liver hypertrophy, some increase in serum cholesterol levels and a small but significant increase in the blood sugar levels were noticed.


1997 ◽  
Vol 272 (1) ◽  
pp. E155-E162 ◽  
Author(s):  
M. K. Hellerstein ◽  
A. Letscher ◽  
J. M. Schwarz ◽  
D. Cesar ◽  
C. H. Shackleton ◽  
...  

We previously described an isotopic method for quantifying the rate of appearance of hepatic UDP-glucose (Ra UDP-Glc) and the direct entry of glucose into hepatic UDP-Glc in humans. Here, the method is tested in depth in rats. The basic principles are that dilution of labeled galactose in hepatic UDP-Glc, sampled noninvasively by the xenobiotic glucuronate (GlcUA) method, reveals Ra UDP-Glc. First, labeling patterns in secreted acetaminophen-GlcUA were compared with hepatic glycogen and plasma glucose by use of mass isotopomer distribution analysis from [2-(13)C]glycerol. Labeling was consistent with common precursor pools of glucose 6-phosphate and triose-phosphate for all end products studied in fasted and in intravenous glucose- and fructose-infused states. Next, [1-(3)H]galactose was administered. After a 24-h fast, Ra UDP-Glc was 25.0 +/- 1.7 mumol.kg body wt-1.min-1 and rose to 57.7 and 72.7 mumol.kg-1.min-1 at intravenous glucose infusion rates of 111 and 167-194 mumol.kg-1.min-1, respectively. Liver glycogen deposition correlated closely with Ra UDP-Glc (R2 = 0.76), although the turnover value was approximately 50% higher than the net deposition rate. In conclusion, the turnover of an intrahepatic metabolite, UDP-Glc, can be measured noninvasively, and Ra UDP-Glc correlates with liver glycogen deposition in rats.


1988 ◽  
Vol 254 (6) ◽  
pp. R969-R976 ◽  
Author(s):  
M. G. Tordoff ◽  
M. I. Friedman

Plasma fuels, pancreatic hormones, liver glycogen, and food and water intake were measured immediately before or during the nocturnal feeding period of rats given hepatic portal or jugular infusions of glucose, fructose, and mannitol (0.3 M x 10 ml/2 h). Compared with mock and saline control infusions, hepatic portal glucose, fructose, and mannitol reliably and equally decreased food intake. Jugular fructose and mannitol also decreased food intake when infused before rats ate but not while they ate. Jugular glucose infusion did not affect food intake. Hepatic portal glucose did not reliably elevate systemic plasma glucose or insulin but increased hepatic glycogen content, indicating that most infused glucose was taken up by the liver. In contrast, jugular glucose increased systemic plasma glucose and insulin but did not affect hepatic glycogen. Hepatic portal fructose decreased plasma ketones and increased triglycerides and liver glycogen. Jugular fructose also decreased ketone levels and tended to increase liver glycogen. Mannitol by either route decreased plasma glucose and increased plasma free fatty acids. These results indicate that hepatic portal infusions that produce changes in plasma fuel concentrations within the physiological range decrease food intake. They strongly suggest this is accomplished by a direct action of the infusates on the metabolism of the liver.


1999 ◽  
Vol 69 (6) ◽  
pp. 403-411 ◽  
Author(s):  
Zulet ◽  
Macarulla ◽  
Higueret ◽  
Martínez

This feeding trial evaluated the influence of a diet containing heated chickpea in a dietary induced rat model of hypercholesterolemia in order to assess some possible protective and therapeutic effects on lipid and carbohydrate metabolism disorders as found with other legumes. Rats fed a diet enriched with coconut oil (25%) and cholesterol (1%) for 42 days (HH) showed a situation of type IIa hyperlipoproteinemia. However, these lipid alterations were improved in the hypercholesterolemic rats receiving control (HC) and legume (HL) diets for 16 days. Moreover, results confirm that the chickpea was more effective than the control diet containing casein in the normalization of triglycerides as well as total and LDL-cholesterol levels. On the other hand, the HH group showed a marked reduction in the liver glycogen content and Glucose-6-Phase activity (involved in glyconeogenesis) and an increase in Glucokinase (GK) activity (involved in glucose utilization). In contrast, the rats receiving chickpea re-established the liver glycogen deposition as compared to the HH group. Also, the chickpea intake increased the GK activity as compared to the control diet. The overall results support that chickpea intake may be recommended in humans with altered lipid profile such as type IIa hyperlipoproteinemia. Additionally, data concerning carbohydrate utilization indicated its potential positive effects in diabetes therapy and their role as biological active food supplements.


1988 ◽  
Vol 256 (2) ◽  
pp. 487-491 ◽  
Author(s):  
A Zorzano ◽  
E Herrera

1. Incorporation of gluconeogenic precursors into blood glucose and hepatic glycogen and acylglycerol glycerol was examined in 24 h-fasted virgin rats by using a flooding procedure for substrate administration. At 10 min after their intravenous injection, the conversion of alanine or glycerol into liver glycogen or acylglycerol glycerol was proportional to glucose synthesis. 2. In 24 h-fasted 21-day-pregnant rats, the incorporation of alanine and glycerol into hepatic acylglycerol glycerol was markedly enhanced compared with the control group. In addition, during fasting at late pregnancy, the proportion of substrates directed to acylglycerol glycerol as compared with the fraction incorporated into glucose was augmented. 3. In pentobarbital-treated fasted rats, the incorporation of both alanine and pyruvate into circulating glucose and into hepatic glycogen and acylglycerol glycerol was increased. Pentobarbital treatment increased the proportion of substrates incorporated into liver glycogen, compared with the fraction appearing in circulating glucose. These changes were concomitant with a marked accumulation of glycogen. 4. The data indicate that, during fasting, gluconeogenesis provides glucose as well as hepatic glycogen and acylglycerol glycerol, independently of whether the substrates enter gluconeogenesis at the level of pyruvate or dihydroxyacetone phosphate.


1960 ◽  
Vol 198 (4) ◽  
pp. 797-799 ◽  
Author(s):  
Nancy G. Boucot ◽  
Elizabeth K. Nurser ◽  
John P. Merrill

In order to evaluate the effects of the chronic uremic syndrome upon some aspects of carbohydrate metabolism in vivo, determinations of gastric and intestinal glucose absorption, and of hepatic glycogen deposition were made in 39 chronically uremic rats and in 49 litter-mate controls. A surgical method for producing chronic uremia was developed. Rats fasted for 24 hours were given a glucose gavage of standard concentration. Three hours later residual gastric and intestinal glucose content and liver glycogen content were determined. No statistically significant difference between the two groups was found in either glucose absorption from the gastrointestinal tract or in glycogen deposition.


1982 ◽  
Vol 56 (4) ◽  
pp. 315-322 ◽  
Author(s):  
C. K. Phares ◽  
Nguyen Duy Ai

ABSTRACTThe effects of infection with plerocercoids of Spirometra mansonoides on tissue glycogen deposition of rats was determined. Hypophysectomized rats infected for two days had higher liver glycogen concentrations than controls and this effect was greatest after one week. Elevated liver glycogen associated with plerocercoid infection was observed in fed animals both at the beginning and at the end of the light period as well as after an overnight fast. Glycogen phosphorylase (1,4αD glucan: orthophosphate α glucosyltransferase EC 2.4.1.1.) was inhibited but glucose-6-phosphatase (EC 3.1.3.9) was unaffected in the livers of infected hypophysectomized rats. While this effect is similar to actions of both growth hormone and insulin, plerocercoid infection had no influence on glycogen of cardiac or skeletal muscle at any time. Plerocercoid infection had no effect on the glycogen concentration of any tissue of intact rats.


1964 ◽  
Vol 207 (2) ◽  
pp. 411-414 ◽  
Author(s):  
Jiro Oyama ◽  
William T. Platt

Unrestrained mice were centrifuged for varying periods ranging from 0.5 to 10 hr at 2.5, 5, and 10 x gravity. Liver glycogen and blood glucose levels increased significantly depending on the g load and exposure time. Adrenalectomy completely abolished the glycogen deposition response. The glycogen response was a critical function of the age of mice; unweaned mice did not respond. Blood corticosterone increased significantly prior to the deposition of glycogen. Centrifuged fed mice deposited three times the amount of glycogen of fasted mice. There was no significant difference in the amount of glycogen deposited in centrifuged mice previously starved for 1, 2, or 3 days. It is concluded that the increased glycogen deposited following centrifugation is effected by an increased elaboration of adrenal corticosterone.


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