scholarly journals Fatty Liver and Kidney Syndrome in Chicks II. Biochemical Role of Biotin

1976 ◽  
Vol 29 (6) ◽  
pp. 429 ◽  
Author(s):  
RL Hood ◽  
A RJohnson ◽  
AC Fogerty ◽  
Judith A Pearson
Keyword(s):  
Fatty Liver ◽  
Pyruvate Carboxylase ◽  
Acetyl Coa Carboxylase ◽  
Defence Mechanisms ◽  
Acetyl Coa ◽  
Liver Size ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Liver And Kidney

The role of biotin-dependent enzymes in the fatty liver and kidney syndrome of young chicks was studied. Under conditions of a marginal deficiency of dietary biotin, the level of biotin in the liver has differing effects on the activities of two biotin-dependent enzymes, pyruvate carboxylase and acetyl-CoA carboxylase. The activity of acetyl-CoA carboxylase is increased, but when the dietary deficiency of biotin produces biotin levels which are below o� 8 p,g/g of liver, the activity of pyruvate carboxylase may be insufficient to completely metabolize pyruvate via gluconeogenesis. There is an increase in liver size and in the activities of enzymes involved in alternate pathways for the removal of pyruvate. Blood lactate accumulates and there is increased synthesis of fatty acids, and an accumulation of palmitoleic acid; these steps are accomplished by increased activities of at least the following enzymes: acetyl-CoA carboxylase, malate dehydrogenase (decarboxylating) (NADP+) and the desaturase enzyme. When the biotin level is below 0�35 p,g/g of liver and the chick is subjected to a stress, physiological defence mechanisms of the chick may be inadequate to maintain homeostasis and they finally collapse, resulting in accumulation of triacylglycerol in the liver and blood; the chick is unable to maintain blood glucose levels and death occurs, often only a few hours after the imposition of the stress.

Abstract 397: HMOX1 Ameliorates Fatty Liver and Metabolic Syndrome by Reduction of Hepatic Heme and PGC1a

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Komal Sodhi ◽  
Wade G Douglas ◽  
Stephen J Peterson ◽  
Larry Dial ◽  
Imran T Khawaja ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Body Weight ◽  
Blood Glucose ◽  
Fatty Liver ◽  
Obese Mice ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Lipid Droplet Size

Introduction: Nonalcoholic fatty liver (NAFLD) occurs in a setting of high fat diets, insulin resistance, obesity and dyslipidemia. Individuals with NAFLD have an increased risk of developing metabolic syndrome. Heme oxygenase-1 (HMOX1), a major cytoprotective enzyme, attenuates oxidative stress and obesity and increases insulin sensitivity. The antioxidant effect of HMOX1 is due to an increase in ferritin, and bilirubin and a decrease in heme, a pro-oxidant. The aim of this study was to examine the role of increased hepatic HMOX activity in decreasing steatosis, adiposity and vascular dysfunction and to determine the mechanism underlying these metabolic changes in obese mice. Methods: Obese mice were administered cobalt protoporphyrin (CoPP) and HMOX activity inhibitor stannous mesoporphyrin (SnMP) for 6 weeks. Blood pressure, body weight and blood glucose levels were measured in all the groups. Glycogen content, hepatic fibrosis, heme levels, fatty acid synthase (FAS) and lipid droplet size in liver were also assessed. Results: CoPP administration increased hepatic HMOX1 protein levels and HMOX activity, decreased blood pressure, body weight, blood glucose levels, hepatic heme content (p<0.05) as compared to obese mice. Our results also showed that HMOX1 induction causes a significant decrease in lipid steatosis ( lipid droplet size and FAS levels; p<0.01) as compared to obese mice. Densitometry analysis showed increased expression of PPARα and Glut 1 along with decreased expression of PGC1α in hepatic tissue. These beneficial effects were reversed by administration of SnMP. Conclusion: This novel study demonstrates the role of hepatic HMOX1 in attenuating the fatty liver and metabolic homeostasis by decreasing PGC1α and heme content and enhancing glycogen levels. Pharmacological agents that increase HMOX1 levels or gene targeting of HMOX1 offer a promising therapeutic target for NAFLD and suggest the existence of a significant link between the heme-HMOX system and the extent and severity of heme-dependent fatty liver.

scholarly journals Fatty Liver and Kidney Syndrome in Chicks I. Effect of Biotin in Diet

1976 ◽  
Vol 29 (6) ◽  
pp. 419 ◽  
Author(s):  
Judith A Pearson ◽  
AR Johnson ◽  
RL Hood ◽  
AC Fogerty
Keyword(s):  
Fatty Acids ◽  
Fatty Liver ◽  
Palmitic Acid ◽  
Palmitoleic Acid ◽  
Saturated Fatty Acids ◽  
Liver Lipids ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Young Parent ◽  
Liver And Kidney

Fatty liver and kidney syndrome, a disorder of young chicks, was studied under laboratory conditions. Affected chicks had enlarged livers (hepatomegaly), an increased content of lipid in the liver, and an increased level of palmitoleic acid in the liver lipids. The disorder was observed mainly in chicks from young parent flocks, and was associated either with commercial diets which were subsequently found to be low in biotin, or with specially formulated low-biotin diets. A third factor, imposition of stress, was required to initiate the disorder. There was evidence of increased lipogenesis causing an increase of triacylglycerols in the liver lipids and an increased production of saturated fatty acids, particularly palmitic acid. Increased levels of palmitoleic acid resulted from an increased desaturation of palmitic acid. Under stress, affected chicks had low blood glucose levels, suggesting that gluconeogenesis was impaired. Since biotin-dependent enzymes are involved in both gluconeogenesis and lipogenesis, it would appear that the relevant enzymes respond differently to a deficiency of biotin.

The role of rice bran extract on acetyl CoA carboxylase in liver of rats fed a high-fat diet

Planta Medica ◽  
2011 ◽  
Vol 77 (12) ◽  
Author(s):  
C Charkhonpunya ◽  
S Sireeratawong ◽  
S Komindr ◽  
N Lerdvuthisopon
Keyword(s):  
Rice Bran ◽  
High Fat Diet ◽  
Acetyl Coa Carboxylase ◽  
High Fat ◽  
Acetyl Coa ◽  
Rice Bran Extract

scholarly journals Role of Insulin in Health and Disease: An Update

2021 ◽  
Vol 22 (12) ◽  
pp. 6403
Author(s):  
Md Saidur Rahman ◽  
Khandkar Shaharina Hossain ◽  
Sharnali Das ◽  
Sushmita Kundu ◽  
Elikanah Olusayo Adegoke ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
Basic Research ◽  
Future Research ◽  
Protective Effects ◽  
Glucose Levels ◽  
Physiological Processes ◽  
Blood Glucose Levels ◽  
Wide Range ◽  
Health And Disease

Insulin is a polypeptide hormone mainly secreted by β cells in the islets of Langerhans of the pancreas. The hormone potentially coordinates with glucagon to modulate blood glucose levels; insulin acts via an anabolic pathway, while glucagon performs catabolic functions. Insulin regulates glucose levels in the bloodstream and induces glucose storage in the liver, muscles, and adipose tissue, resulting in overall weight gain. The modulation of a wide range of physiological processes by insulin makes its synthesis and levels critical in the onset and progression of several chronic diseases. Although clinical and basic research has made significant progress in understanding the role of insulin in several pathophysiological processes, many aspects of these functions have yet to be elucidated. This review provides an update on insulin secretion and regulation, and its physiological roles and functions in different organs and cells, and implications to overall health. We cast light on recent advances in insulin-signaling targeted therapies, the protective effects of insulin signaling activators against disease, and recommendations and directions for future research.

scholarly journals Role of Melanocortin Signaling in Neuroendocrine and Metabolic Actions of Leptin in Male Rats With Uncontrolled Diabetes

Endocrinology ◽  
2014 ◽  
Vol 155 (11) ◽  
pp. 4157-4167 ◽  
Author(s):  
Thomas H. Meek ◽  
Miles E. Matsen ◽  
Vincent Damian ◽  
Alex Cubelo ◽  
Streamson C. Chua ◽  
...  
Keyword(s):  
Male Rats ◽  
Melanocortin Receptor ◽  
Glucose Lowering ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Uncontrolled Diabetes ◽  
Streptozotocin Induced Diabetes ◽  
Melanocortin Signaling ◽  
Antidiabetic Effects

Abstract Although the antidiabetic effects of leptin require intact neuronal melanocortin signaling in rodents with uncontrolled diabetes (uDM), increased melanocortin signaling is not sufficient to mimic leptin's glucose-lowering effects. The current studies were undertaken to clarify the role of melanocortin signaling in leptin's ability to correct metabolic and neuroendocrine disturbances associated with uDM. To accomplish this, bilateral cannulae were implanted in the lateral ventricle of rats with streptozotocin-induced diabetes, and leptin was coinfused with varying doses of the melanocortin 3/4 receptor (MC3/4R) antagonist, SHU9119. An additional cohort of streptozotocin-induced diabetes rats received intracerebroventricular administration of either the MC3/4R agonist, melanotan-II, or its vehicle. Consistent with previous findings, leptin's glucose-lowering effects were blocked by intracerebroventricular SHU9119. In contrast, leptin-mediated suppression of hyperglucagonemia involves both melanocortin dependent and independent mechanisms, and the degree of glucagon inhibition was associated with reduced plasma ketone body levels. Increased central nervous system melanocortin signaling alone fails to mimic leptin's ability to correct any of the metabolic or neuroendocrine disturbances associated with uDM. Moreover, the inability of increased melanocortin signaling to lower diabetic hyperglycemia does not appear to be secondary to release of the endogenous MC3/4R inverse agonist, Agouti-related peptide (AgRP), because AgRP knockout mice did not show increased susceptibility to the antidiabetic effects of increased MC3/4R signaling. Overall, these data suggest that 1) AgRP is not a major driver of diabetic hyperglycemia, 2) mechanisms independent of melanocortin signaling contribute to leptin's antidiabetic effects, and 3) melanocortin receptor blockade dissociates leptin's glucose-lowering effect from its action on other features of uDM, including reversal of hyperglucagonemia and ketosis, suggesting that brain control of ketosis, but not blood glucose levels, is glucagon dependent.

Prediabetes, undiagnosed diabetes and diabetes risk in Italy in 2017–2018: results from the first National screening campaign in community pharmacies

2021 ◽  
Author(s):  
P Brunetti ◽  
L Baldessin ◽  
S Pagliacci
Keyword(s):  
High Risk ◽  
Diabetes Risk ◽  
World Health ◽  
Undiagnosed Diabetes ◽  
Community Pharmacies ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Health Organization ◽  
Very High

Abstract Background Effective policies for diabetes prevention remain urgent. We conducted a mass screening campaign in Italy to identify subjects potentially having undiagnosed diabetes, prediabetes or at diabetes risk. Methods This cohort study was conducted in community pharmacies joining the unitary National federation of pharmacy holders (Federfarma) and participating in the 7-day screening campaign ‘DiaDay’ in 2017–2018. Capillary blood glucose levels and the risk of developing diabetes in 10 years (through the Finnish Diabetes Risk Score) were assessed. Results 145 651 volunteers aged ≥20 years without known diabetes were screened at 5671 community pharmacies in 2017 and 116 097 at 5112 in 2018. Overall, 3.6% had glucose values suggestive of undiagnosed diabetes; under fasting conditions (N = 94 076), 39.9% and 16.4% had values suggestive of prediabetes by the American Diabetes Association and the World Health Organization criteria, respectively. Of those without diabetes (N = 252 440), 19.2% had scores compatible with a high risk (1:3) and 2.7% with a very high risk (1:2) of developing the disease; in the prediabetes group, the risk rose with higher impaired fasting glucose values. Conclusions DiaDay, the first National screening campaign, highlights the need to screen the population and the key role of the pharmacist both in screening activities and education promotion.

The Role of Biomaterials in Insulin Delivery Systems

1980 ◽  
Vol 3 (5) ◽  
pp. 299-304 ◽  
Author(s):  
S.D. Bruck
Keyword(s):  
Blood Glucose ◽  
Glucose Sensor ◽  
Insulin Delivery ◽  
The United States ◽  
Delivery Systems ◽  
Open Loop ◽  
Health Concern ◽  
Glucose Levels ◽  
Blood Glucose Levels

The control of blood glucose levels in diabetes involving devices are critically reviewed, and the role of blood-contacting biomaterial components analyzed. These include mechanical insulin-delivery systems of the closed-loop type that require an electronic glucose sensor and feedback, and open-loop systems that deliver insulin without a sensor and feedback. Whole pancreatic and islet transplantations, islet encapsulation, and the potential role of polymeric sustained drug delivery systems are discussed. The medical and social impacts of diabetes mellitus are of prime public health concern and of even greater magnitude than those of heart disease in the United States. While future advances in device design, miniaturization, and biometrials technology will significantly add to the arsenal of therapeutic alternatives, devices capable of controlling blood glucose levels ought to be viewed as mere interim phases rather than as final goals of the problem.

Liver glycogen content decreases during meals in rats

1982 ◽  
Vol 243 (3) ◽  
pp. R450-R453
Author(s):  
W. Langhans ◽  
N. Geary ◽  
E. Scharrer
Keyword(s):  
Blood Glucose ◽  
Glycogen Content ◽  
Liver Glycogen ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Liver Glycogen Content ◽  
Ad Libitum ◽  
Portal Veins ◽  
Hepatic Portal

The effects of feeding on liver glycogen content and blood glucose in the hepatic and hepatic portal veins were investigated in rats. Liver glycogen content decreased about 25% during meals both in rats refed after 12 h food deprivation (23 +/- 1 to 17 +/- 1 mg glycogen/g liver) and in ad libitum-fed rats taking fully spontaneous meals (44 +/- 2 to 32 +/- 2 mg/g). Liver glycogen began to increase within 30 min after meals in ad libitum-fed rats. Hepatic vein blood glucose levels at meal onset (118 +/- 4 mg/dl in the food-deprived rats, 127 +/- 4 in ad libitum-fed rats) and at meal end (155 +/- 3 and 166 +/- 5 mg/dl, respectively) were similar in the two groups. Portal vein blood glucose increased during meals in the previously food-deprived rats (83 +/- 4 to 116 +/- 6 mg/dl) but not in the ad libitum-fed rats (127 +/- 5 to 132 +/- 3 mg/dl). Mechanisms that may elicit prandial glycogenolysis and the possible role of this effect in the production of meal ending satiety are discussed.

scholarly journals Role of a Novel I1781T Mutation and Other Mechanisms in Conferring Resistance to Acetyl-CoA Carboxylase Inhibiting Herbicides in a Black-Grass Population

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e69568 ◽  
Author(s):  
Shiv Shankhar Kaundun ◽  
Sarah-Jane Hutchings ◽  
Richard P. Dale ◽  
Eddie McIndoe
Keyword(s):  
Acetyl Coa Carboxylase ◽  
Acetyl Coa
Sign in / Sign up

Export Citation Format

Share Document