scholarly journals The activities and intracellular distributions of enzymes of carbohydrate, lipid and ketone-body metabolism in lactating mammary glands from ruminants and non-ruminants

1981 ◽  
Vol 196 (3) ◽  
pp. 747-756 ◽  
Author(s):  
B Crabtree ◽  
D J Taylor ◽  
J E Coombs ◽  
R A Smith ◽  
S P Templer ◽  
...  
Keyword(s):  
Isocitrate Dehydrogenase ◽  
Guinea Pigs ◽  
Ketone Body ◽  
Mammary Glands ◽  
The Other ◽  
Acetyl Coa ◽  
Cytoplasmic Enzyme ◽  
Coa Transferase ◽  
Ketone Body Metabolism ◽  
Rats And Mice

1. The activities of several enzymes of carbohydrate, lipid, acetate and ketone-body metabolism were measured in lactating mammary glands from rats, mice, rabbits, guinea pigs, sows, sheep, cows and goats. The intracellular distributions of many of the enzymes were measured by fractional extraction. 2. Acetyl-CoA synthetase was predominantly cytoplasmic in rats and guinea pigs, but was more mitochondrial in the other species. The different location of this enzyme in rats and mice is discussed in relation to the disposal of reducing equivalents. 3. 3-Oxo acid CoA-transferase and acetoacetyl-CoA thiolase assayed at 600 microM-CoA were predominantly mitochondrial in all species investigated. Acetoacetyl-CoA thiolase assayed at 8 microM-CoA was predominantly cytoplasmic, except in rabbits and guinea pigs. Ruminants appeared to possess little, if any, of the cytoplasmic enzyme. 4. The activities and distributions of NADP-isocitrate dehydrogenase were consistent with a role in supplying cytoplasmic NADPH in ruminant tissue, and indicated that this system may also occur in guinea pigs.

On a Peculiar Type of Intersexuality in the Guinea-Pig

1927 ◽  
Vol 4 (3) ◽  
pp. 227-244
Author(s):  
ALEXANDER LIPSCHUTZ
Keyword(s):  
Guinea Pig ◽  
Guinea Pigs ◽  
Mammary Glands ◽  
The Other ◽  
Normal Male ◽  
Normal Female ◽  
Sexual Hormones ◽  
Testicular Transplantation ◽  
Hereditary Nature ◽  
External Genital Organs

An abnormal condition of the external genital organs in 16 otherwise normal female guinea-pigs is described. They possessed an hypertrophied penis-like clitoris and horny styles similar to those in the intromittent sac of the normal male penis. The abnormalities are often asymmetrical, the clitoris and the horny style on one side being more developed than on the other. They may even be absent on one side. It is suggested that the malformation is a peculiar type of "partial somatic intersexuality," the external genital organs resembling those in the male guinea-pig. The condition is identical with that described in the castrated female guinea-pig experimentally masculinised by testicular transplantation. There was no indication of the ovaries producing simultaneously female and male sexual hormones: (a) The ovaries were histologically normal. (b) The ovaries when engrafted into castrated males produced the typical female hormonic effect on the mammary glands and had no influence on the penis or on the horny styles. (c) The clitoris and the horny styles of the intersexual females were not affected by removal of the ovaries, whereas in the male removal of the testes caused a pronounced regression of the horny styles even in fully grown animals. (d) The horny styles when cut regenerated even after removal of the ovaries; there is never a regeneration in the castrated male, but only in the normal male. The question is discussed whether the described type of intersexuality might be a case of "successive hormonic intersexuality," both kinds of sexual hormones having been produced simultaneously for a certain time whereas at a later stage only female hormones were secreted. The hypertrophied clitoris and the horny styles would then be considered as "fixed" sex characters persisting after the disappearance of the male sexual hormones. The problem of fixation of sex characters by sexual hormones is considered on experimental lines. The facts observed are rather against the suggestion that the intersexuality described is a case of successive hormonic intersexuality. Other possibilities of explaining the morphogenetic basis of this peculiar type of intersexuality are also discussed. The intersexuality described is of an hereditary nature.

THE IN VITRO METABOLISM OF MAMMARY GLAND SLICES IN THE PRESENCE OF POSTERIOR PITUITARY LOBE EXTRACTS RICH IN MELANOPHORE-DISPERSING ACTIVITY

1957 ◽  
Vol 15 (4) ◽  
pp. 366-373 ◽  
Author(s):  
T. R. BRADLEY ◽  
G. M. MITCHELL
Keyword(s):  
Mammary Gland ◽  
Guinea Pigs ◽  
Incubation Medium ◽  
Mammary Glands ◽  
Gas Evolution ◽  
Early Lactation ◽  
Posterior Pituitary ◽  
Rats And Mice ◽  
Posterior Pituitary Lobe

SUMMARY Slices cut from mammary glands of rats and mice during gestation and lactation were incubated in vitro in the presence of pig posterior pituitary lobe extracts rich in melanophore-dispersing ('B') activity. Slices taken in early lactation but not during gestation or late lactation showed increased net gas evolution compared with control slices. Similar tissue from rabbits and guinea-pigs did not give rise to this effect, nor did slices of other tissues taken from lactating rats. The increased net gas evolution was not observed in the absence of glucose from the incubation medium. Treatment of the 'B' extract with NaOH or hypophysectomy of the rats prior to use decreased the response.

scholarly journals Regulation of glucose and ketone-body metabolism in brain of anaesthetized rats

1974 ◽  
Vol 138 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Neil B. Ruderman ◽  
Peter S. Ross ◽  
Michael Berger ◽  
Michael N. Goodman
Keyword(s):  
Glucose Uptake ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Acetyl Coa ◽  
Total Blood ◽  
Diabetic Ketosis ◽  
Pyruvate Oxidation ◽  
Ketone Body Metabolism ◽  
Arteriovenous Difference ◽  
The Brain

1. The effects of starvation and diabetes on brain fuel metabolism were examined by measuring arteriovenous differences for glucose, lactate, acetoacetate and 3-hydroxybutyrate across the brains of anaesthetized fed, starved and diabetic rats. 2. In fed animals glucose represented the sole oxidative fuel of the brain. 3. After 48h of starvation, ketone-body concentrations were about 2mm and ketone-body uptake accounted for 25% of the calculated O2 consumption: the arteriovenous difference for glucose was not diminished, but lactate release was increased, suggesting inhibition of pyruvate oxidation. 4. In severe diabetic ketosis, induced by either streptozotocin or phlorrhizin (total blood ketone bodies >7mm), the uptake of ketone bodies was further increased and accounted for 45% of the brain 's oxidative metabolism, and the arteriovenous difference for glucose was decreased by one-third. The arteriovenous difference for lactate was increased significantly in the phlorrhizin-treated rats. 5. Infusion of 3-hydroxybutyrate into starved rats caused marked increases in the arteriovenous differences for lactate and both ketone bodies. 6. To study the mechanisms of these changes, steady-state concentrations of intermediates and co-factors of the glycolytic pathway were determined in freeze-blown brain. 7. Starved rats had increased concentrations of acetyl-CoA. 8. Rats with diabetic ketosis had increased concentrations of fructose 6-phosphate and decreased concentrations of fructose 1,6-diphosphate, indicating an inhibition of phosphofructokinase. 9. The concentrations of acetyl-CoA, glycogen and citrate, a potent inhibitor of phosphofructokinase, were increased in the streptozotocin-treated rats. 10. The data suggest that cerebral glucose uptake is decreased in diabetic ketoacidosis owing to inhibition of phosphofructokinase as a result of the increase in brain citrate. 11. The inhibition of brain pyruvate oxidation in starvation and diabetes can be related to the accelerated rate of ketone-body metabolism; however, we found no correlation between the decrease in glucose uptake in the diabetic state and the arteriovenous difference for ketone bodies. 12. The data also suggest that the rates of acetoacetate and 3-hydroxybutyrate utilization by brain are governed by their concentrations in plasma. 13. The finding of very low concentrations of acetoacetate and 3-hydroxybutyrate in brain compared with plasma suggests that diffusion across the blood –brain barrier may be the rate-limiting step in their metabolism.

scholarly journals A high-MUFA diet alone does not affect ketone body metabolism, but reduces glycated hemoglobin when combined with exercise training in diabetic rats

2017 ◽  
Vol 9 (1) ◽  
pp. 31-40
Author(s):  
Juraiporn Somboonwong ◽  
Khunkhong Huchaiyaphum ◽  
Onanong Kulaputana ◽  
Phisit Prapunwattana
Keyword(s):  
Exercise Training ◽  
Ketone Body ◽  
Glycated Hemoglobin ◽  
Ketone Bodies ◽  
Transferase Activity ◽  
Nonesterified Fatty Acids ◽  
Regular Diet ◽  
Coa Transferase ◽  
Ketone Body Metabolism ◽  
Mufa Diet

Abstract Background Monounsaturated fat (MUFA) also has glucose-lowering action, but its effect on ketone bodies is unknown. Objectives To examine the effects of high-MUFA diet alone or in combination with exercise training, which can improve glucose and ketone body metabolism, in a rat model of diabetes. Methods Wistar rats were administered streptozotocin to induce diabetes and then randomly divided into five groups: sedentary rats fed a regular diet (1), a high-saturated-fat diet (2), a high-MUFA diet (3); and exercisetrained rats fed a regular diet (4), and a high-MUFA diet (5). Training was by a treadmill twice daily, 5 days/week. At 12 weeks, glucose, glycated hemoglobin (HbA1c), insulin, nonesterified fatty acids (NEFA), and β-hydroxybutyrate levels were measured in cardiac blood. Activity of the overall ketone synthesis pathway was determined in liver and 3-ketoacyl-CoA transferase activity determined in gastrocnemius muscle. Results A high-MUFA diet tended to lower plasma glucose without affecting other biochemical variables. Training did not change glucose metabolism, but significantly reduced serum NEFA. Only the high-MUFA diet plus training significantly decreased HbA1c levels. Hepatic ketone synthesis was decreased and 3-ketoacyl-CoA transferase activity was increased by training alone or in combination with a high-MUFA diet. Changes in NEFA, β-hydroxybutyrate, and the enzymatic activities in response to training plus a high-MUFA diet were comparable to those caused by training alone. Conclusion A high-MUFA diet alone does not alter ketone body metabolism. Combination of a MUFA-rich diet and exercise training is more effective than either MUFA or exercise alone for lowering HbA1c.

scholarly journals Differential Response of Hippocampal and Cerebrocortical Autophagy and Ketone Body Metabolism to the Ketogenic Diet

2021 ◽  
Vol 15 ◽  
Author(s):  
Daniela Liśkiewicz ◽  
Arkadiusz Liśkiewicz ◽  
Marta M. Nowacka-Chmielewska ◽  
Mateusz Grabowski ◽  
Natalia Pondel ◽  
...  
Keyword(s):  
Frontal Cortex ◽  
Ketogenic Diet ◽  
Ketone Body ◽  
Brain Aging ◽  
Ketone Bodies ◽  
Monocarboxylate Transporter ◽  
Proper Function ◽  
Monocarboxylate Transporter 1 ◽  
Coa Transferase ◽  
Ketone Body Metabolism

Experimental and clinical data support the neuroprotective properties of the ketogenic diet and ketone bodies, but there is still a lot to discover to comprehensively understand the underlying mechanisms. Autophagy is a key mechanism for maintaining cell homeostasis, and therefore its proper function is necessary for preventing accelerated brain aging and neurodegeneration. Due to many potential interconnections, it is possible that the stimulation of autophagy may be one of the mediators of the neuroprotection afforded by the ketogenic diet. Recent studies point to possible interconnections between ketone body metabolism and autophagy. It has been shown that autophagy is essential for hepatic and renal ketogenesis in starvation. On the other hand, exogenous ketone bodies modulate autophagy both in vitro and in vivo. Many regional differences occur between brain structures which concern i.e., metabolic responses and autophagy dynamics. The aim of the present study was to evaluate the influence of the ketogenic diet on autophagic markers and the ketone body utilizing and transporting proteins in the hippocampus and frontal cortex. C57BL/6N male mice were fed with two ketogenic chows composed of fat of either animal or plant origins for 4 weeks. Markers of autophagosome formation as well as proteins associated with ketolysis (BDH1—3-hydroxybutyrate dehydrogenase 1, SCOT/OXCT1—succinyl CoA:3-oxoacid CoA transferase), ketone transport (MCT1—monocarboxylate transporter 1) and ketogenesis (HMGCL, HMGCS2) were measured. The hippocampus showed a robust response to nutritional ketosis in both changes in the markers of autophagy as well as the levels of ketone body utilizing and transporting proteins, which was also accompanied by increased concentrations of ketone bodies in this brain structure, while subtle changes were observed in the frontal cortex. The magnitude of the effects was dependent on the type of ketogenic diet used, suggesting that plant fats may exert a more profound effect on the orchestrated upregulation of autophagy and ketone body metabolism markers. The study provides a foundation for a deeper understanding of the possible interconnections between autophagy and the neuroprotective efficacy of nutritional ketosis.

scholarly journals Successful adaptation to ketosis by mice with tissue-specific deficiency of ketone body oxidation

2013 ◽  
Vol 304 (4) ◽  
pp. E363-E374 ◽  
Author(s):  
David G. Cotter ◽  
Rebecca C. Schugar ◽  
Anna E. Wentz ◽  
D. André d'Avignon ◽  
Peter A. Crawford
Keyword(s):  
Ketone Body ◽  
Neonatal Period ◽  
Ketone Bodies ◽  
Fatty Acyl ◽  
Carbohydrate Intake ◽  
Tissue Specific ◽  
Neonatal Mice ◽  
Coa Transferase ◽  
Low Carbohydrate ◽  
Ketone Body Metabolism

During states of low carbohydrate intake, mammalian ketone body metabolism transfers energy substrates originally derived from fatty acyl chains within the liver to extrahepatic organs. We previously demonstrated that the mitochondrial enzyme coenzyme A (CoA) transferase [succinyl-CoA:3-oxoacid CoA transferase (SCOT), encoded by nuclear Oxct1] is required for oxidation of ketone bodies and that germline SCOT-knockout (KO) mice die within 48 h of birth because of hyperketonemic hypoglycemia. Here, we use novel transgenic and tissue-specific SCOT-KO mice to demonstrate that ketone bodies do not serve an obligate energetic role within highly ketolytic tissues during the ketogenic neonatal period or during starvation in the adult. Although transgene-mediated restoration of myocardial CoA transferase in germline SCOT-KO mice is insufficient to prevent lethal hyperketonemic hypoglycemia in the neonatal period, mice lacking CoA transferase selectively within neurons, cardiomyocytes, or skeletal myocytes are all viable as neonates. Like germline SCOT-KO neonatal mice, neonatal mice with neuronal CoA transferase deficiency exhibit increased cerebral glycolysis and glucose oxidation, and, while these neonatal mice exhibit modest hyperketonemia, they do not develop hypoglycemia. As adults, tissue-specific SCOT-KO mice tolerate starvation, exhibiting only modestly increased hyperketonemia. Finally, metabolic analysis of adult germline Oxct1+/− mice demonstrates that global diminution of ketone body oxidation yields hyperketonemia, but hypoglycemia emerges only during a protracted state of low carbohydrate intake. Together, these data suggest that, at the tissue level, ketone bodies are not a required energy substrate in the newborn period or during starvation, but rather that integrated ketone body metabolism mediates adaptation to ketogenic nutrient states.

scholarly journals Why the diabetic heart is energy inefficient: A ketogenesis and ketolysis perspective

2021 ◽  
Author(s):  
Paras Kumar Mishra
Keyword(s):  
Energy Efficiency ◽  
Ketogenic Diet ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Metabolic Flexibility ◽  
Metabolic Abnormalities ◽  
Acetyl Coa ◽  
Cardiac Energy ◽  
Ketone Body Metabolism ◽  
Very High

Lack of glucose uptake compromises metabolic flexibility and reduces energy efficiency in the diabetes mellitus (DM) heart. Although increased utilization of fatty acid to compensate glucose substrate has been studied, less is known about ketone body metabolism in the DM heart. Ketogenic diet reduces obesity, a risk factor for T2DM. How ketogenic diet affects ketone metabolism in the DM heart remains unclear. At the metabolic level, the DM heart differs from the non-DM heart due to altered metabolic substrate and the T1DM heart differs from the T2DM heart due to insulin levels. How these changes affect ketone body metabolism in the DM heart are poorly understood. Ketogenesis produces ketone bodies by utilizing acetyl CoA whereas ketolysis consumes ketone bodies to produce acetyl CoA, showing their opposite roles in the ketone body metabolism. Cardiac-specific transgenic upregulation of ketogenesis enzyme or knockout of ketolysis enzyme causes metabolic abnormalities leading to cardiac dysfunction. Empirical evidence demonstrates upregulated transcription of ketogenesis enzymes, no change in the levels of ketone body transporters, very high levels of ketone bodies, and reduced expression and activity of ketolysis enzymes in the T1DM heart. Based on these observations, I hypothesize that increased transcription and activity of cardiac ketogenesis enzyme suppresses ketolysis enzymes in the DM heart, which decreases cardiac energy efficiency. The T1DM heart exhibits highly upregulated ketogenesis compared to T2DM due to lack of insulin that inhibits ketogenesis enzyme.

Ketone body metabolism in ascorbic acid deficiency: in vivo utilization of ketone bodies in guinea pigs

1959 ◽  
Vol 196 (3) ◽  
pp. 607-610 ◽  
Author(s):  
Habeeb Bacchus ◽  
Albert F. Debons ◽  
Sidney Levin ◽  
John W. Wallace
Keyword(s):  
Ascorbic Acid ◽  
Guinea Pigs ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Deficient Animal ◽  
Ascorbic Acid Deficiency ◽  
Acid Deficiency ◽  
Urinary Levels ◽  
Ketone Body Metabolism

Blood and urinary levels of ketone bodies were studied in normal, ascorbic acid-deficient, and pair-fed control, guinea pigs. The resting levels of ketone bodies in the blood and urine throughout the course of ascorbic acid-deficiency do not differ significantly from those of control animals. The ketonemic response to fasting is greater in the control animals than in the ascorbic acid-deficient animals. The disappearance of injected ketone bodies (ß-hydroxybutyrate) is decreased in the ascorbic acid-deficient animal. The data suggest that in ascorbic acid-deficiency there is a decreased utilization of ketone bodies coupled with a decreased spontaneous ketogenesis.

scholarly journals Hepatic ketone-body metabolism in developing sheep and pregnant ewes

1978 ◽  
Vol 40 (2) ◽  
pp. 359-367 ◽  
Author(s):  
G. Carole E. Varnam ◽  
Marjorie K. Jeacock ◽  
D. A. L. Shepherd
Keyword(s):  
Ketone Body ◽  
Ketone Bodies ◽  
Marked Change ◽  
Acetyl Coa ◽  
Adult Rats ◽  
Adult Sheep ◽  
Pregnant Sheep ◽  
Foetal Life ◽  
Ketone Body Metabolism

1. In order to establish whether or not there is a relationship between the blood ketone-body concentrations and the potential ability of the liver to synthesize ketone bodies in sheep on varying nutritional regimens, a study has been made of the concentrations of acetoacetate and 3-hydroxybutyrate in blood and the activities of enzymes concerned with ketogenesis in liver of developing sheep from mid-way through gestation to maturity, in pregnant ewes from mid-way through pregnancy and in starved pregnant and non-pregnant ewes.2. During development the most marked change in blood 3-hydroxybutyrate concentration occurred when the lambs were weaned. Blood acetoacetate concentrations did not change during development. When mature ewes were starved both 3-hydroxybutyrate and acetoacetate concentrations in blood were increased.3. Changes found in the activity of 3-hydroxybutyrate dehydrogenase (EC 1.1.1.30) in the liver were correlated with the changes in blood 3-hydroxybutyrate concentrations during development but no such relationship existed in pregnant or fasted ewes. No correlation was found between the ability of the liver to synthesize acetoacetate and blood ketone body concentrations in either developing or pregnant adult sheep. The rate of acetoacetate production expressed per g liver increased during foetal life but values observed in lambs 1 d after birth were similar to those found in suckling and mature sheep. During the last month of pregnancy and when non-pregnant sheep were starved the hepatic potential for ketogenesis was increased. During development the activity of acetyl-CoA acetyltransferase (EC 2.3.1.9) was correlated with the rate of hepatic acetoacetate production.4. These changes have been contrasted with those that occur in developing and starved adult rats.5. It is concluded that hepatic production of ketone bodies cannot be the only factor in the regulation of blood ketone body concentrations in developing and pregnant sheep.

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