scholarly journals The response of liver enzymes to feed restriction and subsequent adlib. feeding in the laying hen

1980 ◽  
Vol 44 (1) ◽  
pp. 81-87 ◽  
Author(s):  
J. Pearce
Keyword(s):  
Lipid Metabolism ◽  
Lipid Content ◽  
Food Restriction ◽  
Liver Lipid ◽  
Feed Restriction ◽  
Control Group ◽  
Free Access ◽  
Lipogenic Enzyme ◽  
Liver Lipid Content ◽  
Access To Food

1. The effects of restricted feeding, and ad lib. feeding following food restriction, on hepatic carbohydrate and lipid metabolism in the laying hen were studied.2. The birds were allocated to four groups and given either 92, 84 or 75 g/d or allowed ad lib. access to food.3. Food restriction significantly reduced liver total lipid content compared with ad lib.-fed control birds and this was reflected in reduced hepatic lipogenic enzyme activities.4. When birds from the restricted regimens were allowed free access to food they intially consumed more food than the control group but after 2 weeks of ad lib. feeding the food consumptions of the birds in all the groups were similar.5. Concomitant with the increase in food intake there were also increases in liver lipid content and hepatic lipogenic enzyme activities. After 18 d of ad lib.feeding these measurements were similar in the previously restricted birds and the ad lib.-fed control group.6. Despite these effects on lipid metabolism, food restriction, and the subsequent release from food restriction, had no significant effects on the specific activities of the glycolytic enzymes examined.7. Although there were large increases in liver lipid content following release from feed restriction no birds died from, or showed any of the symptoms of, fatty liver-haemorrhagic syndrome. This suggests that, in the absence of any other factor which may be involved in the syndrome, these high liver lipid contents were not, alone, sufficient to cause FLHS. The results also indicate that free access to food following food restriction is unlikely to be a major factor in initiating the syndrome.

scholarly journals Prenatal hyperandrogenism induces alterations that affect liver lipid metabolism

2016 ◽  
Vol 230 (1) ◽  
pp. 67-79 ◽  
Author(s):  
Giselle Adriana Abruzzese ◽  
Maria Florencia Heber ◽  
Silvana Rocio Ferreira ◽  
Leandro Martin Velez ◽  
Roxana Reynoso ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Metabolism ◽  
Glucose Tolerance ◽  
Fatty Liver ◽  
Lipid Content ◽  
Liver Lipid ◽  
Acid Oxidation ◽  
Liver Lipid Content ◽  
Increased Risk ◽  
Liver Lipid Metabolism

Prenatal hyperandrogenism is hypothesized as one of the main factors contributing to the development of polycystic ovary syndrome (PCOS). PCOS patients have high risk of developing fatty liver and steatosis. This study aimed to evaluate the role of prenatal hyperandrogenism in liver lipid metabolism and fatty liver development. Pregnant rats were hyperandrogenized with testosterone. At pubertal age, the prenatally hyperandrogenized (PH) female offspring displayed both ovulatory (PHov) and anovulatory (PHanov) phenotypes that mimic human PCOS features. We evaluated hepatic transferases, liver lipid content, the balance between lipogenesis and fatty acid oxidation pathway, oxidant/antioxidant balance and proinflammatory status. We also evaluated the general metabolic status through growth rate curve, basal glucose and insulin levels, glucose tolerance test, HOMA-IR index and serum lipid profile. Although neither PH group showed signs of liver lipid content, the lipogenesis and fatty oxidation pathways were altered. The PH groups also showed impaired oxidant/antioxidant balance, a decrease in the proinflammatory pathway (measured by prostaglandin E2 and cyclooxygenase-2 levels), decreased glucose tolerance, imbalance of circulating lipids and increased risk of metabolic syndrome. We conclude that prenatal hyperandrogenism generates both PHov and PHanov phenotypes with signs of liver alterations, imbalance in lipid metabolism and increased risk of developing metabolic syndrome. The anovulatory phenotype showed more alterations in liver lipogenesis and a more impaired balance of insulin and glucose metabolism, being more susceptible to the development of steatosis.

Effect of Methionine on Liver Lipid Content and Lipid Metabolism of Rats Fed a Protein-free Diet

1973 ◽  
Vol 103 (1) ◽  
pp. 54-60 ◽  
Author(s):  
Yoritaka Aoyama ◽  
Masashi Nakanishi ◽  
Kiyoshi Ashida
Keyword(s):  
Lipid Metabolism ◽  
Lipid Content ◽  
Liver Lipid ◽  
Liver Lipid Content ◽  
Protein Free Diet

scholarly journals Apolipoprotein CIII Overexpression-Induced Hypertriglyceridemia Increases Nonalcoholic Fatty Liver Disease in Association with Inflammation and Cell Death

2017 ◽  
Vol 2017 ◽  
pp. 1-18 ◽  
Author(s):  
Adriene A. Paiva ◽  
Helena F. Raposo ◽  
Amarylis C. B. A. Wanschel ◽  
Tarlliza R. Nardelli ◽  
Helena C. F. Oliveira
Keyword(s):  
Cell Death ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Lipid Content ◽  
Fatty Liver Disease ◽  
Liver Lipid ◽  
Hepatic Insulin Resistance ◽  
Nonalcoholic Fatty Liver ◽  
Liver Lipid Content

Nonalcoholic fatty liver disease (NAFLD) is the principal manifestation of liver disease in obesity and metabolic syndrome. By comparing hypertriglyceridemic transgenic mice expressing apolipoprotein (apo) CIII with control nontransgenic (NTg) littermates, we demonstrated that overexpression of apoCIII, independent of a high-fat diet (HFD), produces NAFLD-like features, including increased liver lipid content; decreased antioxidant power; increased expression of TNFα, TNFα receptor, cleaved caspase-1, and interleukin-1β; decreased expression of adiponectin receptor-2; and increased cell death. This phenotype is aggravated and additional NAFLD features are differentially induced in apoCIII mice fed a HFD. HFD induced glucose intolerance together with increased gluconeogenesis, indicating hepatic insulin resistance. Additionally, the HFD led to marked increases in plasma TNFα (8-fold) and IL-6 (60%) in apoCIII mice. Cell death signaling (Bax/Bcl2), effector (caspase-3), and apoptosis were augmented in apoCIII mice regardless of whether a HFD or a low-fat diet was provided. Fenofibrate treatment reversed several of the effects associated with diet and apoCIII expression but did not normalize inflammatory traits even when liver lipid content was fully corrected. These results indicate that apoCIII and/or hypertriglyceridemia plays a major role in liver inflammation and cell death, which in turn increases susceptibility to and the severity of diet-induced NAFLD.

INDUCTION BY GONADAL HORMONES OF HEPATIC LIPOGENIC ENZYME ACTIVITY IN IMMATURE PULLETS

1974 ◽  
Vol 61 (1) ◽  
pp. 29-43 ◽  
Author(s):  
D. BALNAVE ◽  
J. PEARCE
Keyword(s):  
Enzyme Activity ◽  
Corn Oil ◽  
Specific Activity ◽  
Liver Lipid ◽  
Lipogenic Enzyme ◽  
Atp Citrate Lyase ◽  
Liver Lipid Content ◽  
Hormone Administration ◽  
Citrate Lyase ◽  
Specific Activities

SUMMARY The effect of gonadal hormone administration on hepatic lipogenic enzyme activity, and some physiological parameters was investigated in immature pullets. Pullets (aged 4 weeks) were allocated to treatment groups and received intramuscular injections of oestradiol, testosterone, progesterone or oestradiol + testosterone (all in 0·3 ml corn oil) or corn oil alone (control group). There was no evidence of any hormone-induced changes in the specific activity of hepatic ATP-citrate lyase 1, 3, 6 and 12 h after hormone administration. NADP-malate dehydrogenase exhibited significant variations in specific activity over this period of time and it is probable that these changes reflected an increased requirement for NADPH for synthetic purposes in hormone-treated birds. The effect of 1, 2, 4 and 9 days of hormone administration was also investigated. In testosterone-treated birds there were significant increases in the specific activities of both lipogenic enzymes after 1 day of hormone treatment whereas for birds receiving oestradiol the maximum specific activities were found on the second day. Similarly, the liver lipid content of oestradioltreated birds showed a substantial increase on day 2. After 9 days of hormone administration no significant differences in the specific activity of ATP-citrate lyase were observed between treatments but the specific activity of NADP-malate dehydrogenase was significantly reduced in oestradiol- or mixed hormone-treated birds; it is possible that the reduced enzyme activity is associated with a reduced requirement for NADPH and in this connexion there were no further increases in liver lipid content or liver weight after 4 days of hormone administration. The liver RNA:DNA ratio tended to be greatest in birds receiving oestradiol or oestradiol + testosterone. Studies utilizing inhibitors of RNA and protein synthesis showed that such compounds abolished the increases in lipogenic enzyme activity following hormone administration suggesting that these increases were hormone-induced effects. These results are discussed in relation to the effects of the various hormones on liver lipid metabolism and also in relation to the situation in the mature laying hen.

scholarly journals Histological Effect of Allium sativum (Garlic) on the Liver of White Rabbits

2021 ◽  
pp. 28-35
Author(s):  
Osuloye Oluwaseum Olayemi ◽  
Olojo Oluwatobi Omotola ◽  
Philip Abutu
Keyword(s):  
Allium Sativum ◽  
Cell Damage ◽  
Basal Diet ◽  
Liver Glycogen ◽  
Treated Group ◽  
Control Group ◽  
Free Access ◽  
Glycogen Depletion ◽  
Garlic Powder ◽  
Access To Food

Allium sativum commonly referred to as garlic has been known over the years for its medicinal and culinary purposes. It has also been reported to have several toxic effects when used excessively. However, the purpose of this study was to determine the histological effects of Allium sativum (garlic) powder on the liver of white rabbits at different dosages. Twenty rabbits were randomly divided int.o five groups with free access to food and water for a period of four weeks. Four groups B, C, D, and E were fed with garlic supplemented basal diet containing different concentrations of garlic powder i.e. 100mg, 200mg, 500mg, and 1000mg respectively. These groups were called the treated group. Group A was fed with basal diet only and was considered as the control group. The results obtained showed some histological changes such as the presence of cellular necrosis, vacuolations, lipofuscin pigments, pyknosis and nuclear hypertrophy which were as a result of liver glycogen depletion and hepatic cell damage which may be due to relatively high dosage of garlic used in some of the groups.

Effects of ovariectomy and resistance training on lipid content in skeletal muscle, liver, and heart; fat depots; and lipid profile

2009 ◽  
Vol 34 (6) ◽  
pp. 1079-1086 ◽  
Author(s):  
Richard Diego Leite ◽  
Jonato Prestes ◽  
Celene Fernandes Bernardes ◽  
Gilberto Eiji Shiguemoto ◽  
Guilherme Borges Pereira ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Lipid Profile ◽  
Lipid Content ◽  
Liver Lipid ◽  
Atherogenic Index ◽  
Ovariectomized Rats ◽  
Muscle Lipid ◽  
Liver Lipid Content ◽  
Fat Depots

The aim of the present study was to investigate the effects of resistance training on skeletal muscle lipid content, liver lipid content, heart lipid content, fat depots, and lipid profile in ovariectomized rats. Wistar adult female rats were divided into 4 groups (n = 10 per group): sedentary (Sed-Intact), sedentary ovariectomized (Sed-Ovx), strength trained (ChronicEx-intact), and strength trained ovariectomized (ChronicEx-Ovx). A 12-week strength-training period was used, during which the animals climbed a 1.1-m vertical ladder with weights attached to their tails. The sessions were performed once every 3 days, with 4–9 climbs and 8–12 dynamic movements per climb. Ovariectomy increased liver lipid content and fat depots, and heart and muscle lipid content. There was an increase in the atherogenic index and a negative change in lipid profile because of the ovariectomy. Resistance training decreased lipid content in the liver, soleus, and tibialis anterior, decreased fat depots (mesenteric and retroperitoneal), and changed the lipid profile, independently of ovarian hormone status. These results indicate the potential benefits of resistance training as an alternative strategy to control the effects of ovariectomy on fat depot, lipid profile, and tissue lipid content.

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