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Ketogenesis in liver

Ketals, of hexitols, IV, 223 Ketene, acetylation of starch with, I, 290 Keto acids, a- and 0-, specificity of carboxylase action on, V, 50 a-Keto acids, aromatic, V, 50 0-Keto acids, oxidation of, II, 148 a-Ketobutyric acid, V, 50 a-Ketocaproio acids, V, 50 Ketogenesis, in liver slices, II, 155 Ketolysis, II, 120, 146, 147, 158 in liver slices, II, 155 Ketolytic, II, 146... [Pg.370]

In animal cells, fatty acids are degraded both in mitochondria and peroxisomes, whereas in lower eukaryotes, P-oxidation is confined to peroxisomes. Mitochondrial P-oxidation provides energy for oxidative phosphorylation and generates acetyl-CoA for ketogenesis in liver. The oxidation of fatty acids with odd numbers of carbon atoms also yields propi-onyl-CoA that is metabolized to succinate. [Pg.134]

Contrary to popular belief deranged lipid - not carbohydrate - metabohsm is the main cause of DKA. In essence DKA is caused by uncontrolled hpolysis in adipose tissue and uncontrolled ketogenesis in liver. [Pg.34]

Examination of tissues post mortem showed normal acetoacetate oxidation by muscle and normal ketogenesis in liver. The severity of ketosis eliminated non-metabolic causes such as starvation and salicylism, and further investigation of post-mortem tissues for acetoacetyl-CoA thiolase, 3-hydroxybutyrate dehydrogenase and succinyl-CoA 3-keto acid-CoA transferase activities revealed grossly deficient activity of the latter enzyme in brain, kidney, muscle and cultured fibroblasts, in the presence of normal activities of the other enzymes. [Pg.333]

Figure 22-7. Pathways of ketogenesis in the liver. (FFA, free fatty acids HMG, 3-hy-d roxy- 3-m et hy I g I uta ry I.)... Figure 22-7. Pathways of ketogenesis in the liver. (FFA, free fatty acids HMG, 3-hy-d roxy- 3-m et hy I g I uta ry I.)...
Mayes PA, Laker ME Regulation of ketogenesis in the liver. Biochem Soc Trans 1981 9 339. [Pg.189]

Answer C. Severe hypoglycemia lowers the insulin level and increases glucagon. This would favor fatty acid release from the adipose and ketogenesis in the liver. [Pg.160]

Lipoaldehydes, II, 123 Lipositol, III, 47, 343 Lithium aluminum hydride, for hydrogenation of 1,2-epoxides, V, 22 Lithium chloride, influence upon the activity of pancreatic amylase, V, 237 Lithium hypochlorite, III, 137 Liver, fat conversion by isolated, II, 141 ketogenesis in isolated, II, 155 Lobry de Bruyn-Alberda van Ekenstein transformation, III, 113 Locust bean mucilage, IV, 267 Lucerne seed, emulsins, V, 63 Lucerne seed, mucilage, IV, 266, 267 Lupinus albus, galactan from seed of, II, 248... [Pg.372]

Figure 32-5. P-oxidation and ketogenesis in the liver. The rate-limiting step in fatty acid oxidation and subsequent ketone body production is the activity of carnitine acyltrans-ferase I (CAT I).The activity of CAT I is inhibited by malonyl-CoA. Insulin deficiency results in inhibition of acetyl-CoA carboxylase, decreased levels of maloyl-CoA, and thus increased activity of CAT-I.Adapted from Foster and McGarry (1983). Figure 32-5. P-oxidation and ketogenesis in the liver. The rate-limiting step in fatty acid oxidation and subsequent ketone body production is the activity of carnitine acyltrans-ferase I (CAT I).The activity of CAT I is inhibited by malonyl-CoA. Insulin deficiency results in inhibition of acetyl-CoA carboxylase, decreased levels of maloyl-CoA, and thus increased activity of CAT-I.Adapted from Foster and McGarry (1983).
Thurston JH and Hauhart RE (1992) Amelioration of adverse effects of valproic acid on ketogenesis and liver coenzyme A metabolism by cotreatment with pantothenate and carnitine in developing mice possible clinical significance. Pediatric Research 31, 419-23. [Pg.455]

In patients with diabetes plus liver cirrhosis, acarbose treatment appears to be favourable because it improves the detoxification of ammonia (Muting, 1984). Acarbose induces an increased growth of lactobacteria, lowers intestinal pH and hyperammonaemia, inducing a beneficial effect on portosystemic encephalopathy. It also reduces lipolysis and ketogenesis in cirrhotic patients (Zillikens et at., 1989), following a late evening meal with 100 mg acarbose. [Pg.169]

Ketogenesis in the liver. All reactions occur in mitochondria the rate-controlling reactions (not shown) are release of fatty acids from adipose tissue and uptake of acyl-CoA into mitochondria, in particular, the CPTI reaction (see Figure 18-1). Acetoacetyl-CoA may regulate ketogenesis by inhibiting the transferase and the synthase. [Pg.377]

Woifrum, C., Asiimaz, E., Luca, E., Friedman, J. M., and Stoffel, M. Foxa2 regulates lipid metabolism and ketogenesis in the liver during fasting and in diabetes. Nature 432 (2004) 1027-1032. [Pg.47]

Additional information <2, 6> (<6> enzyme functions as a metabolic sensor that monitors cellular AMP and ATP levels [31] <2> phosphory-lates key target proteins that control flux through metabolic pathways of hepatic ketogenesis, cholesterol synthesis, adipocyte lipolysis and skeletal muscle fatty acid oxidation [30] <4> regulates triacylglycerolsynthesis and fatty acid oxidation in liver and muscle reciprocally [29]) [29-31]... [Pg.469]

Fatty Acid Oxidation and Ketogenesis in Rat Liver under Proliferation of Mitochondria and Peroxisomes... [Pg.125]

Yamanaka, H., Ueshima, Y, Nakajima, T., Yoshida, N., Inoue, F, Kodo, N., Kinugasa, A. Sawada, T. (1992)7. InheritedMetab. Dis., 15, 353-355. Gluconeogenesis and ketogenesis in perfused livers from short-chain acyl-CoA dehydrogenase-deficient mice. [Pg.402]


See other pages where Ketogenesis in liver is mentioned: [Pg.394]    [Pg.394]    [Pg.185]    [Pg.236]    [Pg.172]    [Pg.174]    [Pg.144]    [Pg.366]    [Pg.231]    [Pg.113]    [Pg.388]    [Pg.388]    [Pg.388]    [Pg.875]    [Pg.155]    [Pg.157]    [Pg.766]    [Pg.115]    [Pg.133]    [Pg.144]    [Pg.144]    [Pg.2157]    [Pg.467]    [Pg.320]    [Pg.164]    [Pg.229]    [Pg.240]    [Pg.246]   
See also in sourсe #XX -- [ Pg.372 , Pg.373 ]




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