Glycerol Feeding Research Articles

Sleep changes in fasting rats after chronic glycerol feeding

Species which do not enter torpor during fasting and which were efficiently able to spare their body proteins during the first two phases of fasting (which are commonly comprised of 3 successive phases) also increase their daily amount of slow-wave sleep (SWS) during the first two phases. Since in fasting animals the ability to spare proteins was reported to be improved when they were previously fed with a diet enriched with glycerol, it was supposed that, after such a diet, food-deprived rats would increase their daily quota of SWS. In addition, the tolerance to food deprivation, defined as the time elapsed to reach the end of phase II, should also be improved since this tolerance is known to be critically modulated by protein utilization. The daily proportions of wakefulness (W), SWS and paradoxical sleep (PS) were thus studied in Wistar rats after 16 weeks of feeding (i.e., when they were 27 weeks old) with an enriched glycerol diet. These daily W and sleep state proportions were then evaluated until the middle of fasting phase II (MII), i.e., when protein catabolism in the rat appears to be at its lowest level. The rats were able to tolerate more than 5 weeks of food deprivation, which represented an increase of 123% of the fasting tolerance previously reported in rats of the same age but which were fed normally before fasting onset. At MII the daily proportion of SWS was significantly (vs. fed state, p<0.01) increased (due to an increase in the daily mean episode duration), at the expense of W (due to a lowering in the daily occurrence of W episodes). During fasting, the daily amounts of PS remained roughly constant. The hypothesis relating the fasting tolerance to the rate of change observed in the daily amount of SWS still remains valuable even when the normal fasting tolerance is altered. The possible adaptative value connected to the change in the sleep-waking pattern of the present fasting rats is also discussed.

Phosphate sequestration by glycerol and its effects on photosynthetic carbon assimilation by leaves

Glycerol induced a limitation on photosynthetic carbon assimilation by phosphate when supplied to leaves of barley (Hordeum vulgare L.) and spinach (Spinacia oleracea L.). This limitation by phosphate was evidenced by (i) reversibility of the inhibition of photosynthesis by glycerol by feeding orthophosphate (ii) a decrease in light-saturated rates of photosynthesis and saturation at a lower irradiance, (iii) the promotion of oscillations in photosynthetic CO2 assimilation and in chlorophyll fluorescence, (iv) decreases in the pools of hexose monophosphates and triose phosphates and increases in the ratio of glycerate-3-phosphate to triose phosphate, (v) decreased photochemical quenching of chlorophyll fluorescence, and increased non-photochemical quenching, specifically of the component which relaxed rapidly, indicating that thylakoid energisation had increased. In barley there was a massive accumulation of glycerol-3-phosphate and an increase in the period of the oscillations, but in spinach the accumulation of glycerol-3-phosphate was comparatively slight. The mechanism(s) by which glycerol feeding affects photosynthetic carbon assimilation are discussed in the light of these results.

Effect of glycerol feeding on endurance and metabolism during prolonged exercise in man

This study evaluated the effectiveness of pre-exercise glycerol feeding in protecting against development of hypoglycemia and sparing muscle glycogen during prolonged, intense exercise. Thirty minutes after ingesting either glycerol (1 gm X kg-1 body weight) or a placebo, 10 cyclists performed as much exercise on a cycle ergometer as they were able in 150 min. The average exercise intensity was 72% of VO2max during both trials. Glycerol ingestion increased blood glycerol concentration 100-fold, but did not alter the respiratory exchange ratio (R), plasma levels of insulin and free-fatty acids, or blood lactate and beta-hydroxybutyrate. The only significant effect of glycerol feeding was to postpone the decline in blood glucose by about 30 min. This suggests that glycerol served, to a limited extent, as a gluconeogenic substrate; however, glycerol ingestion did not spare muscle glycogen during 90 min of treadmill exercise at 71% VO2max. It appears that man cannot utilize glycerol as gluconeogenic substrate rapidly enough to serve as a major energy source during strenuous exercise.

Effects of glycerol feeding before and after exhausting exercise in rats.

Rats were fed either 1 g of glycerol or 1 g of glucose following exercise to exhaustion. Glucose feeding resulted in a rapid increase in blood glucose, with attainment of peak hyperglycemia within 1 h and of peak muscle glycogen in about 2 h. Feeding 1 g of glycerol resulted in marked elevation of glycerol concentration in blood, liver, and muscle; the highest values, measured 1 h after glycerol feeding, ranged from 29 to 42 mumol/g tissue. Blood glucose and muscle glycogen increased slowly in the glycerol-fed rats and peaked much later than after glucose feeding. In perfused rat hindlimb muscles, negligible amounts of [14C]glycerol were incorporated into glycogen. These findings suggest that muscle is not able to utilize glycerol to a significant extent and that glucose derived from glycerol was the major substrate for muscle glycogen synthesis. Animals fed glycerol before a run to exhaustion were able to exercise significantly longer than control rats (153 +/- 11 min vs. 116 +/- 6 min). The glycerol-fed rats depleted their muscle and liver glycogen stores less rapidly than the controls and were protected against development of hypoglycemia during the exercise.

Effect of glycerol on triglyceride metabolism in the rat

Lipid metabolic studies were carried out on the male Wistar rats fed on glycerol-rich diet in order to elucidate the mechanism of glycerol-induced hypertriglyceridemia. No difference was found between the glycerol fed rats and the control rats in the rate of triglyceride secretion from the liver measured by the Triton WR-1339 method as well as in the rate of incorporation of labeled glycerol into liver triglyceride. The facts that the half-life of the intravenously injected intralipid ® in the blood was significantly delayed in the glycerol fed rats and that the lipoprotein lipase activity released from epididymal adipose tissue of the glycerol fed rats was markedly decreased to 19% of that of the control rats seem to account for the serum triglyceride elevation induced by the glycerol feeding.

The microbial metabolism of cyclohexylacetic acid [proceedings

glycerol feeding of starved pups resulted in an increase in hepatic acetyl-CoA (27,umoI/ g), a decrease in the NAD+/NADH ratio in cytosol and mitochondria, and completely reversed the two limiting steps of gluconeogenesis. This suggests that oxidation of fatty acids is essential for efficient gluconeogenesis in the liver of newborn rats by providing acetyl-CoA, an activator of mitochondria1 pyruvate carboxylase, and by providing reducing equivalents (NADH) to displace the cytosolic glyceraldehyde phosphate dehydrogenase reaction towards glucose synthesis.

Effect of Glycerol on Lipogenic Enzyme Activities and on Fatty Acid Synthesis in the Rat and Chicken

The influence of glycerol on the rates of fatty acid snythesis in liver slices from rats and chickens in pieces of adipose tissue from rats was first studied. Then the effect of dietary glycerol on lipid metabolism in rats and cheickens was examined. Media containing 3 or 10 mM glycerol depressed the rate of glucose conversion to fatty acids in rat liver slices. However, media containing up to 25 mM glycerol did not influence the rate of fatty acid synthesis in chick liver slices. The inhibitory action of glycerol in rat liver slices might occur at the level of glucose (or glycogen) conversion to pyruvate because glycerol did not inhibit pyruvate or acetate conversion to fatty acids. Rats and chickens were fed glycerol containing diets for either 3 days or 3 weeks. Feeding diets containing 20.5 parts glycerol (22% of dietary energy) to rats or chickens did not influence the growth rate of the animals. However, substitution of 42.2 parts glycerol (43% of dietary energy) for glucose in the diet significantly depressed food intake and growth rate in both rats and chickens. The activities of citrate cleavage enzyme, fatty acid synthetase and malic enzyme in livers of rats fed the glycerol-containing diets were dramatically increased. However, this stimulation of enzyme activity occurred without a concomitant increase in the in vivo rate of fatty acid synthesis in the rat liver. In the chicken, unlike the rat, dietary glycerol did not stimulate but instead decreased hepatic malic enzyme and fatty acid synthetase activities. No significant differences in adipose tissue lipogenic enzyme activities or in the rates of fatty acid synthesis were observed in rats fed glycerol-containing diets. The lipogenic response to glycerol feeding depends on the species as well as the organ.

INTERRELATIONSHIPS BETWEEN BLOOD METABOLITES AND AN EVALUATION OF THEIR USE AS CRITERIA OF ENERGY STATUS OF COWS IN EARLY LACTATION

Correlation and regression coefficients were calculated for blood metabolites, milk components, energy balance and efficiency of energy utilization for a total of 120 cows. The animals were on propylene glycol and glycerol feeding experiments, and correlation coefficients were calculated for combinations of parameters with the objective of assessing the effect of additive and level of additive on the constancy of these relationships. In order to attempt an explanation of the variation in relationships between treatment groups, two groups each comprising 19 animals were chosen, based on blood ketone body levels. These groups provided a comparison between stressed (ketotic) and non-stressed (control) animals. Blood glucose was more highly correlated with acetoacetate and β-hydroxybutyrate than with free fatty acids when calculated for treatment groups. When calculated for the two selected groups, significant correlations (P &lt; 0.01) for glucose vs. acetoacetate, β-hydroxybutyrate and free fatty acids were −0.56, −0.61 and −0.28, respectively, for the ketotic group. No significant correlations (P &gt; 0.05) were found between these parameters in the control group. The correlations between blood glucose, acetoacetate and β-hydroxybutyrate and energy balance were very low. Plasma-free fatty acid levels were more closely associated with energy balance than were the other blood metabolites. When energy balance and free fatty acid correlations were compared for ketotic and control groups, only the control group showed a significant (P &lt; 0.01) coefficient (r = − 0.42). The correlation between mean plasma-free fatty acids and mean body weight change over the experimental period for all animals, with time and treatment effects removed, was significant (r = − 0.54, P &lt; 0.01). The estimated free fatty acid level at zero body weight change was 0.53 μ eq per ml plasma. It is concluded that although free fatty acid levels are more sensitive than glucose as an indicator of energy status of the lactating cow, the excessive variability of this relationship during early lactation drastically limits its usefulness.

The effect of controlled feeding of glycerol on beta-galactosidase production by Escherichia coli in batch culture.

AbstractA mutant of E. coli constitutive for β‐galactosidase has been grown in batch culture with the carbon source, glycerol, fed at various fixed rates to the culture. High feeding rates where growth was only slightly restricted gave final enzyme levels similar to those obtained in cultures where all the glycerol was added initially. Low feeding rates resulted in breakdown of the β‐galactosidase formed and gave reduced final levels of the enzyme.

Hormonal and dietary control of enzymes in the rat. IV. Dietary control of some liver enzymes unique to amino acid metabolism and gluconeogenesis and its dependence on pancreatic hormones.

The adaptability of rat liver enzymes involved in amino acid catabolism and gluco-neogensis was examined in response to feeding glucogenic substrates. Feeding of lactate and glycerol inhibited an increase in serine dehydratase [EC 4. 2.1.13] activity caused by starvation. Phosphoenolpyruvate carboxykinase [EC 4.1.1. 32] and tyrosine transaminase [EC 2. 6.1. 5] activities remained low on feeding glycerol but not lactate. Feeding of glucogenic amino acids did not differentially depress the enzyme activities tested. Serine dehydratase activity was markedly enhanced by feeding alanine rather than lowered. Thus the effects of glucogenic substrates on enzymes catalyzing amino acid degradation and gluconeogenesis are partly differential but not strictly. Then it was tested whether pancreatic hormones are involved in enzyme regulation by nutrients. Serine dehydratase was not induced by amino acid-feeding in pancreatectomized rats. Tyrosine transaminase could be induced by amino acid-feeding even in the absence of all of the pancreatic, adrenocortical, and hypophyseal hormones. The role of pancreas in this connection was demonstrated by pancre-atectomy of hypophysectomized rats to be in the maintenance of the enzyme levels and stimulation of the enzyme induction by amino acid-feeding. The effects of glucagon and an amino acid mixture on tyrosine transaminase were additive in hypophysectomized-pancreatectomized rats. Phosphoenolpyruvate carboxykinase activity in pancreatectomized rats was depressed by feeding of glycerol and more consistently by combined administration of glycerol and insulin.

Diet, muscle glycogen, and endurance performance.

Diet, muscle glycogen, and endurance performance.

Production and catabolite repression of the constitutive polygalacturonic acid trans-eliminase of Aeromonas liquefaciens.

Production of polygalacturonic acid (PGA) trans-eliminase was greatly stimulated under conditions of restricted growth of Aeromonas liquefaciens. This was accomplished either by substrate restriction in a continuous-feeding culture or by restricting divalent cations in a batch culture, with the use of PGA as the sole source of carbon in a chemically defined medium containing inorganic nitrogen. Slow feeding of glucose, glycerol, or PGA to carbon-limited cultures allowed PGA trans-eliminase to be formed at a maximum differential rate 500 times greater than in batch cultures with excess substrate present. The differential rate of enzyme formation obtained by slow feeding of these three substrances or of a mixture of PGA plus glucose was observed to be the same. Therefore, PGA trans-eliminase produced by A. liquefaciens, contrary to the current view, appears to be constitutive. These observations also indicate that production of PGA trans-eliminase is subject to catabolite repression and that limiting the substrate reverses this repression. It was also found that, under conditions of unrestricted growth, any compound which the bacteria can use as a source of carbon and energy repressed constitutive PGA trans-eliminase production. The heritable reversal of catabolite repression of PGA trans-eliminase synthesis was demonstrated by isolation of mutant strain Gc-6 which can readily synthesize the constitutive catabolic enzyme PGA trans-eliminase while growing in the presence of excess substrate.

Dietary response of various key enzymes related to glucose metabolism in normal and diabetic rat liver

With normal rats, administration of a high glycerol diet for 3 days produces a great increase in the activities of various key enzymes involved in glucose utilization in the liver. These include glucokinase (EC 2.7.1.12), pyruvate kinase (EC 2.7.1.40), glucose-6-phosphate dehydrogenase (EC 1.1.1.49), ATP citrate lyase (EC 4.1.3.8) and acetyl-CoA carboxylase (EC 6.4.1.2). Administration of a high glycerol diet to diabetic animals also causes a marked induction of all these enzymes, except glucokinase and glucose-6-phosphate dehydrogenase, in the liver. The latter two enzymes show little response to glycerol feeding in the diabetic state. The induction of pyruvate kinase nd ATP citrate lyase by glycerol feeding is almost completely abolished by actinomycin D treatment in both normal and diabetic rats. The elevated activities of glucose-6-phosphatase (EC 3.1.3.9) and l-serine dehydratase (EC 4.2.1.13) in diabetic liver are not lowered but rather increase on feeding glycerol. A possible explanation for these results is presented, especially in relation to the action of insulin.

Hyperglyceridemia induced by glycerol feeding

The currently prevailing opinion is that the endogenous plasma triglycerides have their main if not sole origin in the liver. In the hepatic triglyceride synthesis the precursor fatty acids come chiefly from the body free fatty acid pool and the glycerol moiety is apparently derived both from body free glycerol pool and from the 3-carbon compounds of the glycolysis occuring in hepatic cell. Knowledge of the factors which determine and control the rates of hepatic and plasma triglyceride synthesis is so far very incomplete. One of these factors probably is the plasma free fatty acid level (2) but experience on ethanol-induced fatty liver and hyperglyceridemia (4) as well as on high-carbohydrate diet-induced hyperglyceridemia (7) clearly indicates that the regulatory mechanism must be more complex. In a previous study we suggested that the concentration and synthesis rate of ▪-glycerophosphate in the liver cell or in some of its subcellular fractions might be one of the determinants of triglyceride formation (4). This concept has been supported, in a way, by the recent results of Tzur et al. (6). Since the liver ▪-glycerophosphate content can be raised manifold by administration of glycerol it seemed of interest to study whether the plasma and liver lipid levels are influenced by chronic glycerol feeding in the rat.

The isolation of glycerol-fermenting and lipolytic bacteria from the rumen of the sheep.

SUMMARY: Facultatively anaerobic bacteria appear to play little part in glycerol fermentation in the sheep rumen. Amongst the most important members of the glycerol-fermenting flora are strict anaerobes of the group Selenomonas ruminantium var. lactilyticas. Three isolates of a different group of strictly anaerobic curved Gram-negative rods, which hydrolyse linseed oil and tributyrin as well as fermenting glycerol, were obtained in numbers which suggest they are amongst the more important lipolytic bacteria in the rumen. The main product of fermentation of glycerol by the seleno-monads and the lipolytic bacteria is propionic acid, but other acids are also formed. The properties of these bacteria and some others isolated during the experiments are described. All the bacteria appear to be normal inhabitants of the rumen of sheep fed a number of different rations. The numbers of these organisms were not appreciably increased by feeding glycerol or triglycerides to the animals.

Depression in Percentage of Milk Fat by Parenteral Glucose Infusion and Glycerol Feeding

Low roughage–high concentrate diets can profoundly depress the fat content of milk1–6. One of us has advanced the hypothesis6 that such depressions are the result of metabolic effects of an increase in the proportion of glycogenic to non-glycogenic products of digestion on such diets. Such an increase could be effected by a proportion of the starch escaping ruminal digestion, high ruminal lactic acid production, and an increased proportion of the glycogenic propionic acid in the products of ruminal digestion. There is evidence that low roughage–high concentrate diets have such effects5,7,8. It is also known that the proportions of fat and carbohydrate in the diet of animals can profoundly affect their carbohydrate and lipid metabolism, and changes, although erratic, in blood lipids have been recorded on low roughage diets5,9, indicating some disturbance of lipid metabolism.