Metabolic fuel homeostasis in golden hamsters: effects of fasting, refeeding, glucose, and insulin

1984 ◽  
Vol 247 (1) ◽  
pp. R57-R62 ◽  
Author(s):  
N. Rowland
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Glycogen Content ◽  
Liver Glycogen ◽  
Acid Synthesis ◽  
Ingestive Behavior ◽  
Metabolic Responses ◽  
Exogenous Insulin ◽  
Rapid Reversal

Experiments were conducted to investigate possible metabolic correlates of the unusual ingestive behavior of hamsters after food deprivation. A hypothesis of metabolic refractoriness predicts that hamsters, unlike rats, should not show changes in plasma metabolic fuels, adipose tissue, or liver after fasting and subsequent refeeding. This hypothesis was discredited by findings that fasted hamsters, like rats, have increased plasma ketones and free fatty acids and decreased liver glycogen. On refeeding, hamsters showed rapid reversal of these changes, with supranormal glycogen content and apparent fatty acid synthesis in liver. Additional studies examined the metabolic responses of hamsters and rats to exogenous insulin or glucose administration. Incorporation of 3H2O into liver fatty acids was greatly elevated in rats by both insulin and glucose, but in hamsters only insulin was effective. Some of these metabolic differences may help our understanding of the unusual refractoriness of hamster food intake to various stimuli.

The 1990 Borden Award Lecture Dietary regulation of fatty acid and triglyceride metabolism

1991 ◽  
Vol 69 (11) ◽  
pp. 1637-1647 ◽  
Author(s):  
Gene R. Herzberg
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipoprotein Lipase ◽  
Fatty Acid Synthesis ◽  
Dietary Fat ◽  
Acid Synthesis ◽  
Fish Oils ◽  
Dietary Fish

The level of circulating triacylglycerols is determined by the balance between their delivery into the plasma and their removal from it. Plasma triacylglycerols are derived either from dietary fat as chylomicrons or from endogenous hepatic synthesis as very low density lipoproteins. Their removal occurs through the action of lipoprotein lipase after which the fatty acids are either stored in adipose tissue or oxidized, primarily in skeletal muscle and heart. The composition of the diet has been shown to influence many of these processes. Hepatic fatty acid synthesis and triacylglycerol secretion are affected by the quantity and composition of dietary fat, carbohydrate, and protein. Polyunsaturated but not saturated fats reduce hepatic fatty acid synthesis by decreasing the amount of the lipogenic enzymes needed for de novo fatty acid synthesis. Dietary fish oils are particularly effective at reducing both fatty acid synthesis and triacylglycerol secretion and as a result are hypotriacylglycerolemic, particularly in hypertriacylglycerolemic individuals. In addition, dietary fish oils can increase the oxidation of fatty acids and lead to increased activity of lipoprotein lipase in skeletal muscle and heart. It appears that the hypotriacylglycerolemic effect of dietary fish oils is mediated by effects on both synthesis and removal of circulating triacylglycerols.Key words: lipid, fish oil, fructose, liver, adipose tissue, oxidation.

LIPOGENESIS IN ADIPOSE TISSUE OF MEAL-FED RATS: A POSSIBLE REGULATORY ROLE OF α-GLYCEROPHOSPHATE FORMATION

1967 ◽  
Vol 45 (2) ◽  
pp. 201-214 ◽  
Author(s):  
Gilbert A. Leveille
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Incubation Medium ◽  
Control Mechanism ◽  
Acid Synthesis ◽  
Fatty Acyl ◽  
Epididymal Adipose Tissue ◽  
Malic Dehydrogenase

The incorporation of acetate-1-14C into fatty acids by isolated epididymal adipose tissue of fed and fasted rats adapted to a single daily 2-hour meal (meal eaters) or fed ad libitum (nibblers) was investigated. Fasting (22 hours) markedly depressed lipogenesis whereas fatty acid synthesis increased linearly with time of refeeding in meal-fed but not in nibbling rats. The activities of glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and NADP-malic dehydrogenase in adipose tissue of meal-fed or nibbling rats were not altered as a consequence of a 22-hour fast or of subsequent feeding for 2 hours. The incorporation of acetate-1-l4C into fatty acids by adipose tissue of fasted meal-eating or nibbling animals was markedly enhanced by the addition of unlabeled pyruvate or oxaloacetate to the incubation medium. This stimulatory effect was not observed with adipose tissue front fed meal-eating rats. The addition of unlabeled glucose and insulin to the incubation medium markedly enhanced acetate-1-14C incorporation into fatty acids by isolated adipose tissue and completely overcame any effect of fasting. Adipose tissue converted pyruvate-1-14C, -2-14C, or -3-14C to fatty acids and glyceride-glycerol. The results obtained are consistent with the functioning of a pathway in adipose tissue involving mitochondrial carboxylation of pyruvate to oxaloacetate, and equilibration of the newly formed oxaloacetate with malate and fumarate, followed by cytoplasmic conversion of oxaloacetate to phosphoenol pyruvate. The data are interpreted to support a control mechanism in which fatty acid synthesis is inhibited by tissue fatty acids and fatty acyl-CoA derivatives. The inhibition could in turn be reduced by the availability of α-glycerophosphate, for the esterification of fatty acids. This control mechanism is proposed as the explanation for the refeeding response observed in adipose tissue of meal-fed rats.

Effects of pregnancy and ovarian steroids on fatty acid synthesis and uptake in Syrian hamsters

1991 ◽  
Vol 260 (1) ◽  
pp. R153-R158 ◽  
Author(s):  
A. J. Bhatia ◽  
G. N. Wade
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
White Adipose Tissue ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Acid Synthesis ◽  
De Novo Lipogenesis ◽  
Ovarian Steroids ◽  
Syrian Hamsters

The effects of pregnancy and ovarian steroids on the in vivo distribution of newly synthesized fatty acids (incorporation of tritium from 3H2O into fatty acid) in Syrian hamsters (Mesocricetus auratus) were examined. During late, but not early, gestation hamsters had reduced levels of newly synthesized fatty acids in heart, liver, uterus, and white adipose tissues (parametrial and inguinal fat pads). Treatment of ovariectomized hamsters with estradiol + progesterone significantly decreased fatty acid synthesis-uptake in heart, liver, and inguinal white adipose tissue. Treatment with either estradiol or progesterone alone was without significant effect in any tissue. Pretreatment of hamsters with Triton WR-1339 (tyloxapol), an inhibitor of lipoprotein lipase activity and tissue triglyceride uptake, abolished the effects of estradiol + progesterone in white adipose tissue and heart but not in liver. Thus hamsters lose body fat during pregnancy in part because of decreased de novo lipogenesis. The effect of pregnancy on lipogenesis is mimicked by treatment with estradiol + progesterone but not by either hormone alone. Furthermore, it appears that the liver is the principal site of estradiol + progesterone action on lipogenesis in Syrian hamsters.

Probing metabolic memory in the hepatic response to fasting

2020 ◽  
Vol 52 (12) ◽  
pp. 602-617
Author(s):  
Merel Defour ◽  
Guido J. E. J. Hooiveld ◽  
Michel van Weeghel ◽  
Sander Kersten
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Human Liver ◽  
Tca Cycle ◽  
Liver Glycogen ◽  
Acid Synthesis ◽  
Liver Cells ◽  
Metabolic Memory ◽  
Human Liver Cells ◽  
Glucose Plasma

Tissues may respond differently to a particular stimulus if they have been previously exposed to that same stimulus. Here, we tested the hypothesis that a strong metabolic stimulus such as fasting may influence the hepatic response to a subsequent fast and thus elicit a memory effect. Overnight fasting in mice significantly increased plasma free fatty acids, glycerol, β-hydroxybutyrate, and liver triglycerides, and decreased plasma glucose, plasma triglycerides, and liver glycogen levels. In addition, fasting dramatically changed the liver transcriptome, upregulating genes involved in gluconeogenesis and in uptake, oxidation, storage, and mobilization of fatty acids, and downregulating genes involved in fatty acid synthesis, fatty acid elongation/desaturation, and cholesterol synthesis. Fasting also markedly impacted the liver metabolome, causing a decrease in the levels of numerous amino acids, glycolytic-intermediates, TCA cycle intermediates, and nucleotides. However, these fasting-induced changes were unaffected by two previous overnight fasts. Also, no significant effect was observed of prior fasting on glucose tolerance. Finally, analysis of the effect of fasting on the transcriptome in hepatocyte humanized mouse livers indicated modest similarity in gene regulation in mouse and human liver cells. In general, genes involved in metabolic pathways were upregulated or downregulated to a lesser extent in human liver cells than in mouse liver cells. In conclusion, we found that previous exposure to fasting in mice did not influence the hepatic response to a subsequent fast, arguing against the concept of metabolic memory in the liver. Our data provide a useful resource for the study of liver metabolism during fasting.

scholarly journals Utilization of methylmalonate for the synthesis of branched-chain fatty acids by preparations of chicken liver and sheep adipose tissue

1978 ◽  
Vol 176 (3) ◽  
pp. 799-804 ◽  
Author(s):  
J R Scaife ◽  
K W J Wahle ◽  
G A Garton
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Complex Mixture ◽  
Acid Synthesis ◽  
Inhibitory Effect ◽  
Chicken Liver ◽  
Malonyl Coa ◽  
Branched Chain

1. The utilization of methyl[2-14C]malonyl-CoA for fatty acid synthesis was investigated using synthetase preparations from chicken liver and sheep adipose tissue. 2. The rate of fatty acid synthesis from acetyl-CoA and malonyl-CoA was greatly diminished in the presence of methylmalonyl-CoA. 3. In the absence of malonyl-CoA, methylmalonyl-CoA was utilized for fatty acid synthesis only very slowly by the synthetase from sheep adipose tissue and not at all by that from chicken liver. 4. Despite the inhibitory effect of methylmalonyl-CoA on fatty acid synthesis from malonyl-CoA, it was utilized by the synthetase preparations from both species to produce a complex mixture of methyl-branched fatty acids.

EFFECTS OF HIGH LEVELS OF DIETARY COPPER ON ENDOGENOUS LIPID METABOLISM IN THE PIG

1972 ◽  
Vol 52 (1) ◽  
pp. 113-123 ◽  
Author(s):  
A. W. MYRES ◽  
J. P. BOWLAND
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Unsaturated Fatty Acids ◽  
Acid Synthesis ◽  
Dietary Copper ◽  
Plasma Triglycerides ◽  
Plasma Fraction ◽  
Endogenous Lipid

Two experiments were carried out to study the effects of dietary copper on the performance and lipid metabolism of pigs. In experiment 1 the addition of 250 ppm copper had no significant effect on performance but resulted in a more unsaturated depot fat. It was postulated that the latter effect could be caused by a preferential mobilization of saturated fatty acid (SFA) from adipose tissue, but examination of the fasting free fatty acid (FFA) plasma fraction revealed no evidence for any preferential mobilization, although the concentration of total FFA was increased in the copper-fed animals. The objective of experiment 2 was to investigate whether dietary copper resulted in an increased synthesis of unsaturated fatty acids (UFA) in adipose tissue. Uptake of plasma triglycerides was prevented by prior injection of Triton WR-1339 to give an uncomplicated picture of fatty acid synthesis. The results showed that copper did alter the distribution of 14C activity in adipose tissue fatty acids but shifted the pattern to one of a more saturated nature, which clearly invalidated the hypothesis that copper increases synthesis of UFA.

The effects of pregnancy, lactation and involution on the metabolism of glucose by rat parametrial adipose tissue

1973 ◽  
Vol 40 (3) ◽  
pp. 353-360 ◽  
Author(s):  
R. W. Smith
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Acid Synthesis ◽  
Fat Depots ◽  
Phosphogluconate Dehydrogenase ◽  
Total Body Fat ◽  
Pregnancy And Lactation ◽  
Total Body ◽  
Glucose 6 Phosphate Dehydrogenase

SummaryThe incorporation of 14C from [1-14C] and [6-14C]glucose into CO2, fatty acids and glycerol by rat parametrial adipose tissue was measured at intervals during pregnancy, lactation and involution. There were small increases in the incorporation of both the C-1 and C-6 atoms into CO2 and glycerol on the seventh and sixteenth days of pregnancy. Fatty acid synthesis from glucose was negligible on the twentieth day of pregnancy and during lactation. Three days after weaning the rate of oxidation of the C-1 atom was doubled and the incorporation of both carbon atoms into fatty acids was increased at least 20-fold. There were no changes in the activities of glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase during pregnancy and lactation, but 3 days after weaning the activities of both enzymes were doubled. These results are discussed in relation to other evidence that the total body fat is increased during pregnancy, and to the idea that the fat depots are mobilized during lactation.

scholarly journals The effect of body condition on metabolic changes associated with intake of food by the cow

1983 ◽  
Vol 50 (1) ◽  
pp. 81-89 ◽  
Author(s):  
J. A. Bines ◽  
S. V. Morant
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Rumen Fluid ◽  
Acid Synthesis ◽  
Blood Levels ◽  
Rapid Rate ◽  
Short Term ◽  
Esterified Fatty Acids ◽  
Lower Blood

1. Changes in concentrations of metabolites in blood and rumen fluid were measured in cows when fat and when thin and when given hay and concentrates at a restricted level or ad lib.2. When fed ad lib., cows consumed 24% more food when thin than when fat.3. Concentrations in rumen fluid of acetate and propionate after feeding at both levels did not differ significantly between fat and thin cows.4. Concentrations in blood of the lipogenic substrates acetate and 3-hydroxybutyrate did not differ between fat and thin cows after feeding, but glucose concentration fell more rapidly in thin cows especially when fed ad lib. Propionate rose more in thin cows than in fat cows when fed ad lib. Non-esterified fatty acids were higher in fat cows before feeding, but fell to similar levels to those in thin cows after feeding.5. The results are interpreted as indicating a more rapid rate of fatty acid synthesis in adipose tissue of thin cows. This in turn tends to lower blood levels of fatty acid precursors and so enhance the rate of their absorption from the rumen. This in turn permits higher intake of food before short-term chemical regulators of intake start to operate.

scholarly journals Fatty acid synthesis in liver and adipose tissue of normal and genetically obese (ob/ob) mice during the 24-hour cycle

1975 ◽  
Vol 150 (2) ◽  
pp. 167-173 ◽  
Author(s):  
D A Hems ◽  
E A Rath ◽  
T R Verrinder
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Dark Period ◽  
Acid Synthesis ◽  
Obese Mice ◽  
Total Rate ◽  
Relative Significance ◽  
Adipose Organ

1. The synthesis of long-chain fatty acids de novo was measured in the liver and in regions of adipose tissue in intact normal and genetically obses mice throughout the daily 24h cycle. 2. The total rate of synthesis, as measured by the rate of incorporation of 3H from 3H2O into fatty acid, was highest during the dark period, in liver and adipose tissue of lean or obese mice. 3. The rate of incorporation of 14C from [U-14C]glucose into fatty acid was also followed (in the same mice). The 14C/3H ratios were higher by a factor of 5-20 in parametrial and scapular fat than that in liver. This difference was less marked during the dark period (of maximum fatty acid synthesis). 4. In normal mice, the total rate of fatty acid synthesis in the liver was about twofold greater than that in all adipose tissue regions combined. 5. In obese mice, the rate of fatty acid synthesis was more rapid than in lean mice, in both liver and adipose tissue. Most of the extra lipogenesis occurred in adipose tissue. The extra hepatic fatty acids synthesized in obese mice were located in triglyceride rather than phospholipid. 6. In adipose tissue of normal mice, the rate of fatty acid synthesis was most rapid in the intra-abdominal areas and in brown fat. In obese mice, all regions exhibited rapid rates of fatty acid synthesis. 7. These results shed light on the relative significance of liver and adipose tissue (i.e. the adipose ‘organ’) in fatty acid synthesis in mice, on the mino importance of glucose in hepatic lipogenesis, and on the alterations in the rate of fatty acid synthesis in genetically obese mice.

scholarly journals Fatty acid synthesis in the regenerating liver of the rat

1978 ◽  
Vol 170 (1) ◽  
pp. 1-8 ◽  
Author(s):  
C D Gove ◽  
D A Hems
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Partial Hepatectomy ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Plasma Concentrations ◽  
Liver Glycogen ◽  
Acid Synthesis ◽  
Liver Cholesterol ◽  
Regenerating Liver

1. Synthesis de novo of fatty acids in the rat liver, measured per g wet wt. of tissue, was increased by a factor of about two, between 1 and 4 days after partial hepatectomy, compared with rates in sham-operated control rat livers. 2. There were no associated changes in the rates of liver cholesterol synthesis or of adipose-tissue fatty acid synthesis in rats after partial hepatectomy, compared with rates in sham-operated rats. 3. In regenerating livers, perfused under three different conditions, there was no alteration in the capacity for fatty acid synthesis compared with that of control rats. 4. The increased synthesis of fatty acids in regenerating liver was associated with insignificant increases in plasma concentrations of tricylglycerols and free fatty acids, with a decrease in content of liver glycogen, and with no change in hepatic activity of acetyl-CoA carboxylase. 5. The accelerated rate of synthesis of fatty adids in regenerating liver appears not to be due to any intrinsic alteration in hepatic capacity for fatty acid synthesis, but it may be caused by the continuous action on liver of unidentified circulating factors.

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