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PubMed1964

CELLULAR LIPIDS OF A NOCARDIA GROWN ON PROPANE AND N-BUTANE.

Lipid fractions of propane- and n-butane-grown nocardial cells each contain a chloroform-soluble, ether-insoluble polymer not observed previously in liquid n-alkane-grown cells. The polymer in propane-grown cells is poly-beta-hydroxybutyrate. The polymer in n-butane-grown cells apparently contains unsaturation in the molecule, and is identified tentatively as a co-polymer of beta-hydroxybutyric and beta-hydroxybutenoic (specifically 3-hydroxy 2-butenoic) acids. The other major component of the lipid fraction consists of triglycerides containing principally palmitic and stearic acids. There seems to be little qualitative distinction in the glycerides of propane- or n-butane-grown cells. Oxidative assimilation of n-butane is described.

Butanes↗

PubMed1968

Mechanism of alpha-glycerophosphate regulation of acetyl-coenzyme A carboxylase of Saccharomyces cerevisiae.

The mechanism proposed for the activation of animal acetyl-coenzyme A (CoA) carboxylase by alpha-glycerophosphate, namely, the removal of inhibitory palmityl-CoA via glyceride synthesis, is not the only possible one in the yeast system because extracts exhibiting marked stimulation of acetyl-CoA carboxylase activity by alpha-glyerophosphate show a lack of acyl-CoA compounds.

Citrates↗

PubMed1968

Lipolytic esterases in staphylococci.

Staphylococci split a wide range of lipid substrates by production of an enzyme complex with two main components (i) a lipase acting optimally on fat-soluble glycerides, and (ii) an esterase acting optimally on water-soluble esters. The action is dependent upon carbon chain length, interfacial dispersion, solubility, and pH of substrate and end products. The esterase is less susceptible to organophosphorus inhibitors than mammalian esterases. There is no apparent correlation between lipolysis and markers of pathogenicity such as production of coagulase and toxin, but the possession of a flexible lipolytic mechanism might account for the persistence of staphylococci in the fatty secretions of mammalian skin.

Esterases↗

PubMed1974

Regulatory defect of glycolysis in human lipoma.

A metabolic defect has been observed in extracts of lipomata in which citrate fails to inhibit the conversion of glucose-6-phosphate to glyceride-glycerol. Phospho-fructokinase extracted from lipomata was less sensitive to inhibition by citrate than the enzyme of normal adipose tissue. However, maximal rates of lipogenesis (from glucose or palmitate) and lipolysis (stimulated with isoprenaline) in lipomata were similar to those of normal adipose tissue. This work suggests that loss of negative feedback control of regulatory enzymes may be an early feature in the development of neoplasia.

Adipose Tissue↗

PubMed1976

Lipid metabolism in Achlya: studies of lipid turnover during development.

The life cycle of Achlya involves germination of spores to form coenocytic somatic hyphae, followed by differentiation of hyphal tips into sporangia. From germination to release of new spores occupies 27-30 h. Total lipid made up 10% of dry weight in ungerminated spores. After germination, total lipid fell to 6% of dry weight in 15 h, then rose to 7.7% at the time of sporangium formation. Half of the initial loss of lipid took place within 2 h of germination. The ability of Achlya to incorporate [1-14C]acetate into lipid was maximal at the time of sporangium formation, and glycerides were the principal component of total lipid to become 14C-labelled at all stages of the life cycle. Fatty acid synthetase activity measured in cell-free extracts was low in spores and in actively elongating mycelium, but increased during idfferentiation to a level 15-fold greater than that in spores. Fatty acid oxidation, as estimated by the release of 14CO2 from 1-14C-labelled fatty acids, was also maximal at the time of sporangium formation.

Acetates↗

PubMed1985

Lipid profiles of Aspergillus niger and its unsaturated fatty acid auxotroph, UFA2.

A comparative study of the mycelial lipid composition of a wild strain (V35) and one unsaturated fatty acid auxotroph (UFA2) of Aspergillus niger has been performed. The lipid composition of both strains are qualitatively the same but quantitatively different. All the strains contain the following phospholipids: cardiolipin, phosphatidylethanolamine, phosphatidylcholine, lysophosphatidylethanolamine, lysophosphatidylcholine, and phosphatidylserine; and triglycerides, diglycerides, monoglycerides, ergosterol, and sterol esters as the neutral lipids; mono- and di-galactosyl diglyceride as the major glycolipids along with small amounts of the corresponding mannose analogs. Phosphatidylethanolamine and phosphatidylcholine constitute the bulk of the phospholipids. The mutant (UFA2) contains a higher level of glycerides and lower levels of sterol (both free and esterified form), phospholipids, and glycolipids than the wild type. Aspergillus niger contains C16 to C18 saturated and unsaturated fatty acids. Small amounts of long-chain (C20 to C24) and short-chain (C10 to C14) saturated and unsaturated acids are also present. Linoleic, oleic, and palmitic are the major acids, stearic and linolenic acids being minor ones. UFA2 grows only in the presence of unsaturated fatty acid (C16 or C18) and accumulates a higher concentration of supplemented acid which influences its fatty acid profile.

Aspergillus niger↗

PubMed1985

A radioisotopic technique for analysis of free fatty acid reesterification in human adipose tissue.

Reesterification rates of free fatty acids (FFA) formed by intracellular triglyceride hydrolysis in small fragments of human adipose tissue were measured. Subcutaneous gluteal adipose tissue, obtained by needle biopsy, was incubated in a buffered albumin medium containing [3H]palmitate and [14C]glucose, each of high specific activity. In triglycerides (TG) and diglycerides (DG) synthesized by the tissue, [14C]glucose is incorporated exclusively into the glyceride-glycerol moiety, and 3H appears solely in the esterified fatty acids. Since rates of TG and DG synthesis can be determined from 14C accumulation rates in these molecules, the total amounts of FFA esterified can also be calculated. The difference between this estimate of total FFA esterification and the moles of [3H]palmitate esterified to these molecules represents the amount of unlabeled FFA from ongoing TG hydrolysis that was reesterified during the incubation. FFA recycling by the reesterification pathway is an important mechanism for the control of the quantity and proportions of FFA and glycerol leaving the human adipocyte. Fasting and beta-adrenergic stimulation reduce the fraction of endogenously released FFA that are reesterified from resting values of 30-40% to 8-21%, thereby increasing the molar ratio of FFA to glycerol leaving the adipocyte. The technique described can be employed to monitor sequential changes in this important metabolic cycle in humans under a wide range of nutritional and clinical circumstances.

Adipose Tissue↗

PubMed2003

Expression of glycerokinase in brown adipose tissue is stimulated by the sympathetic nervous system.

The effect of cold exposure (4 degrees C) or prolonged norepinephrine infusion on the activity and mRNA levels of glycerokinase (GyK) was investigated in rat interscapular brown adipose tissue (BAT). Cold exposure for 12 and 24 h induced increases of 30% and 100%, respectively, in the activity of BAT GyK, which was paralleled by twofold and fourfold increase in enzyme mRNA levels. BAT hemidenervation resulted in reductions of 50% and 30% in GyK activity and in mRNA levels, respectively, in denervated pads from rats kept at 25 degrees C, and suppressed in these pads the cold-induced increases in both GyK activity and mRNA levels. The increase in GyK activity induced by cold exposure was not affected by phenoxybenzamine, but was markedly inhibited by previous administration of propranolol or actinomycin D. BAT GyK activity did not change significantly after 6 h of continuous subcutaneous infusion of norepinephrine (20 microg/h), but increased twofold and fourfold after 12 and 24 h, with no further increase after 72 h of infusion. Norepinephrine infusion also activated mRNA production, but the effect was comparatively smaller than that on enzyme activity. beta-Adrenergic agonists also stimulated GyK activity with the following relative magnitude of response: CL316243 (beta(3)) > isoproterenol (non-selective) > dobutamine (beta(1)). In vitro rates of incorporation of glycerol into glyceride-glycerol were increased in BAT from rats exposed to cold. The data suggest that in conditions of a sustained increase in BAT sympathetic flow there is a stimulation of GyK gene expression at the pretranslational level, with increased enzyme activity, mediated by beta-adrenoreceptors, mainly beta(3).

Adipose Tissue, Brown↗

PubMed1976

Prolactin and testicular lipids.

The effects of prolactin and prolactin plus progesterone (P-P) on the testes of adult rats were investigated. The weight of testes, seminal vesicles and the lipid composition of testes were studied 24 h after the administration of hormones. Prolactin treatment increased the weight of seminal vesicles but did not affect testicular weight, whereas P-P treatment had markedly reduced the weights of testes and seminal vesicles. Progesterone did not have any effect on the weight of testes and seminal vesicles. Both treatments had significantly reduced the total testicular lipids, which was more pronounced in the P-P treated group (28, 50%, respectively). The esterified cholesterol was increased by the administration of prolactin and P-P with a concurrent fall in the free cholesterol. The total cholesterol was depleted only by prolactin treatment. Testicular phospholipids, particularly the phosphatidylcholine and phosphatidylethanolamine were markedly depleted by these hormones. This action of prolactin is more significant in the presence of progesterone. The depletion of phospholipids appears to be mainly due to enhanced flow of testicular tubular fluid carrying away phospholipids from testis rather than a shift in the biosynthetic pathway favouring glyceride formation. In our previous study, it has been shown that progesterone favours accumulation of esterified cholesterol by depleting the available free cholesterol. Prolactin on the other hand depletes phospholipids and total cholesterol, increases esterified cholesterol. Thus, prolactin appears to have a role in steroidogensis as well as in the secretory processes of the testis.

Animals↗

PubMed1977

Lipids in human testis.

The lipid composition of human testis intesticular and post-testicular causes of infertility was studied. The testicular causes of infertility was represented by patients with adult seminiferous tubule failure and Klinefelter's syndrome. The post-testicular causes of infertility were represented by patients with obstruction of efferent ducts of testes. A significant accumulation of total testicular lipids was observed in both causes of infertility. A marked increase in free and esterified cholesterol, monoglycerides and triglycerides caused the accumulation of total testicular lipids in testicular causes of infertility. The accumulation of these lipids was more pronounced in Klinefelter's syndrome compared to adult seminiferous tubule failure. In post-testicular causes of infertility, a vary marked increase in phospholipids along with cholesterol fractions and glycerides led to the accumulation of total testicular lipids. The significant increase in total phospholipids caused by the increases in phosphatidylcholine and phosphatidylethanolamine differentiates post-testicular causes of infertility from testicular causes in which phospholipid classes remained unaffected. Thus, changes in hormonal mileu due to pathological conditions also lead to marked alterations in testicular lipids.

Adolescent↗

PubMed1972

Metabolic relationships among the plasma lipoproteins. Reciprocal changes in the concentrations of very low and low density lipoproteins in man.

The changes in other plasma lipoproteins which accompany alterations in very low density lipoproteins (VLDL) were studied in 31 normal and hyperlipidemic men and women who underwent weight reduction, carbohydrate induction, or clofibrate treatment. Plasma lipids and individual lipoprotein cholesterol concentrations were measured serially during control and treatment periods. Low density lipoprotein (LDL) protein was determined by radial immunodiffusion. Oppositely directed changes in VLDL and LDL were found with each of the three metabolic perturbations. Changes in high density lipoprotein (HDL) cholesterol generally paralleled those in LDL but were less consistent. Two patients with type III hyperlipoproteinemia failed to demonstrate reciprocal increases in LDL despite more than 40% reduction in plasma glycerides or VLDL with weight reduction or clofibrate therapy. After clofibrate therapy, LDL increased in proportion to the absolute decrease in VLDL cholesterol during treatment. LDL protein changed relatively less than did LDL cholesterol. The mechanism for the interdependency of plasma VLDL and LDL concentrations over the long term is not known and may be the result of altered rates of interconversion of these lipoproteins, or to feedback inhibition by VLDL of LDL production and release.

Adolescent↗

PubMed1973

Lingual lipase and its role in the digestion of dietary lipid.

The serous glands of rat tongue were found to contain a potent lipolytic enzyme which hydrolyzed triglyceride to mostly diglyceride and free fatty acids (FFA) at pH 4.5-5.4. Homogenates of lingual serous glands from adult rats hydrolyzed 40-70 mmol of triglyceride/g per h. The soft palate, anterior oral pharyngeal wall, and lateral oral pharyngeal glands also contained the activity, but at a much lower level. The lipolytic activity was also found in saliva collected through an esophageal cannula and in stomach contents of rats fed a fat-rich meal. The stomach contained very little activity, however, when saliva was excluded. Lipolytic activity was not found in the stomach wall or in the parotid, submandibular, and sublingual glands. The findings suggest that the lingual serous glands secrete a lipase which catalyzes in the stomach the conversion of triglyceride to partial glycerides and FFA. It is proposed that this reaction is the first step in the digestion of dietary lipid.

Animals↗

PubMed1985

Inhibition of vasopressin-stimulated water flow in toad bladder by phorbol myristate acetate, dioctanoylglycerol, and RHC-80267. Evidence for modulation of action of vasopressin by protein kinase C.

The action of vasopressin (AVP) in transporting epithelia is mediated by cyclic AMP(cAMP), whereas its effects in hepatocytes are mediated by calcium and phosphoinositides. Based on our recent observation that AVP stimulates phosphoinositide turnover in toad bladder, we examined the role of calcium-phospholipid-dependent kinase (protein kinase C) as a modulator of AVP's hydroosmotic effect. Phorbol myristate acetate (PMA), which can substitute for diglyceride as an activator of protein kinase C, the diglyceride dioctanoylglycerol, and RHC-80267, a glyceride lipase inhibitor that should increase diglyceride levels, inhibited AVP-stimulated water flow, but not water flow stimulated by cAMP, suggesting inhibition of cyclic AMP production. Both the dioctanoylglycerol and RHC-80267, but not PMA, also decreased water flow in response to 8-bromo cAMP indicating a potential inhibition at post-cAMP events as well. PMA increased prostaglandin synthesis; however, inhibition of water flow persisted even when prostaglandin synthesis was completely blocked by incubation with naproxen. Furthermore, water flow was not inhibited by incubation with the inactive diglyceride substitute phorbol didecanoate, supporting the specificity of the PMA inhibition. Consistent with the site of action at adenylate cyclase suggested by the transport experiments, PMA and RHC-80237 decreased both cell cAMP content and the cyclic AMP-dependent kinase ratio (-cAMP/+cAMP), an index of intracellular cyclic AMP effect. Assay for protein kinase C activity in toad bladder epithelial cell supernatant demonstrated that the toad bladder indeed contains a kinase stimulable by phospholipid, calcium, and PMA. As an apparently independent effect, we found that addition of PMA, but not dioctanoylglycerol or RHC-80267, to the mucosal bath increased both water permeability and the frequency of granular cell luminal membrane aggregates in the absence of vasopressin, consistent with stimulation of fusion events at the luminal membrane. Our data suggest that protein kinase C can modulate AVP-stimulated water flow in toad bladder by inhibiting cAMP generation, and perhaps post-cAMP steps as well, and support the hypothesis that AVP-stimulated turnover of membrane phosphoinositides antagonize the effects of AVP via changes in diglyceride, calcium, and protein kinase C.

Animals↗

PubMed2002

In-vitro release and oral bioactivity of insulin in diabetic rats using nanocapsules dispersed in biocompatible microemulsion.

This study evaluated the potential of poly(iso-butyl cyanoacrylate) (PBCA) nanocapsules dispersed in a biocompatible microemulsion to facilitate the absorption of insulin following intragastric administration to diabetic rats. Insulin-loaded PBCA nanocapsules were prepared in-situ in a biocompatible water-in-oil microemulsion by interfacial polymerisation. The microemulsion consisted of a mixture of medium-chain mono-, di- and tri-glycerides as the oil component, polysorbate 80 and sorbitan mono-oleate as surfactants and an aqueous solution of insulin. Resulting nanocapsules were approximately 200 nm in diameter and demonstrated a high efficiency of insulin entrapment (> 80%). In-vitro release studies showed that PBCA nanocapsules could suppress insulin release in acidic media and that release at near neutral conditions could be manipulated by varying the amount of monomer used for polymerisation. Subcutaneous administration of insulin-loaded nanocapsules to diabetic rats demonstrated that the bioactivity of insulin was largely retained following this method of preparing peptide-loaded nanocapsules and that the pharmacodynamic response was dependent on the amount of monomer used for polymerisation. The intragastric administration of insulin-loaded nanocapsules dispersed in the biocompatible microemulsion resulted in a significantly greater reduction in blood glucose levels of diabetic rats than an aqueous insulin solution or insulin formulated in the same microemulsion. This study demonstrates that the formulation of peptides within PBCA nanocapsules that are administered dispersed in a microemulsion can facilitate the oral absorption of encapsulated peptide. Such a system can be prepared in-situ by the interfacial polymerisation of a water-in-oil biocompatible microemulsion.

Administration, Oral↗

PubMed2004

Studies on the intestinal absorption of low molecular weight heparin using saturated fatty acids and their derivatives as an absorption enhancer in rats.

Intestinal absorption of low molecular weight heparin (LMWH) as well as unfractionated heparin (UFH) is limited due to its large molecular size and extensive negative charge. Development of its oral formulations would allow outpatient treatment with LMWH and UFH, and contribute a reduction in hospital expenses. The present study was aimed at evaluating the absorption enhancers Labrasol and Gelucire 44/14, which mainly consist of glycerides and fatty acids esters, to improve the intestinal absorption of LMWH. The absorption effects of saturated fatty acids with several carbon chain lengths (C6-C14) were also investigated. LMWH formulated with or without absorption enhancer was administered to the duodenum of fasted rats. The doses of LMWH and absorption enhancer were 20 mg/kg and 30 mg/kg, respectively. Plasma anti-Xa activity was measured as a marker of the LMWH absorption. By administration of the LMWH formulation with Labrasol but not with Gelucire 44/14, the plasma anti-Xa activity was increased to a level above 0.2 IU/ml which is the critical level for elucidation of its anticoagulant activity. Saturated fatty acids also enhanced the intestinal absorption of LMWH, and the order of absorption-enhancing effect was C10=C12>C14>C16>C8> or =C6. These results suggest that the intestinal absorption of LMWH varies with carbon chain lengths of the saturated fatty acids.

Adjuvants, Pharmaceutic↗

PubMed1988

Lymphatic absorption of hypolipidemic compound, 1-O-[p-(myristyloxy)-alpha-methylcinnamoyl] glycerol (LK-903).

The intestinal absorption process of 1-O-[p-(myristyloxy)-alpha-methylcinnamoyl] glycerol (LK-903), a new hypolipidemic compound, was studied in rats. When 3H-LK-903 or 3H-LKA [3H-p- (myristyloxy)-alpha-methyl cinnamic acid], labeled at the cinnamic acid moiety, or 14C-LK-903, labeled at the glycerol moiety, were administered orally to thoracic duct-cannulated rats at a dose of 0.233 mmol/kg, 31.1, 6.7 and 18.1% of the dose, respectively, appeared in the lymph within 24 h. In this case, radioactive compounds in the lymph lipids consisted of LKA (radioactivity was not detected in the fraction of LKA with 14C-LK-903), LK-903, diglyceride analogues and triglyceride analogues. The percentages of the triglyceride analogues were the highest, followed by the diglyceride analogues. On the other hand, when doubly labeled LK-903 (3H/14C = 1, corrected ratio) was administered orally, the values of 3H/14C for the monoglyceride, diglyceride and triglyceride analogues in the lymph were 1.2-1.5, 1.7-1.9 and 1.9-2.7, respectively. The lymphatic absorption of LK-903 was stimulated by the presence of lecithin but inhibited by a high dose of triolein. The results indicated that (1) LK-903 formed micelles in the intestine, (2) a large part of LK-903 was absorbed as such, (3) a part of LK-903 was hydrolyzed in the intestinal mucosa, and (4) a part of LKA formed by hydrolysis was again utilized to synthesize the higher glycerides and absorbed via the lymphatic absorption route for lipids.

Animals↗

PubMed1991

Role of prolactin on Leydig, Sertoli and germ cellular neutral lipids in bonnet monkeys, Macaca radiata.

To elucidate the specific influence of prolactin on neutral lipids in Leydig, Sertoli and germ cell compartments of the testis in immature and mature monkeys, the present study was carried out by injecting ovine prolactin (oPRL) (1 mg/kg body weight/twice daily for 10 days ip), to both age groups. Similarly, bromocryptine (an ergot alkaloid which inhibits prolactin secretion) was given to other sets of immature and mature monkeys (1 mg/kg body weight/twice daily for 10 days ip) to induce hypoprolactinemia. It was observed that after oPRL administration the total lipid accumulated in the germ cells of immature and mature monkeys. Total lipid was markedly decreased in the Leydig cells of mature monkeys only. But no such influence of PRL was evident in the Leydig cells of immature monkeys, suggesting an age-dependent effect of PRL on the Leydig cells. The increase in total lipid in the germ cells following PRL treatment was contributed by mono, di- and triacyl glycerols and free cholesterol. However, an opposite effect of PRL was evident in the Leydig cells of mature monkeys, where the cholesterols and glyceride fractions registered a decrease. The reduced cholesterol fractions in the Leydig cells following PRL treatment suggests the utilization of cholesterol for steroidogenesis. Sertoli cells were found to be comparatively resistant to change in PRL status. Bromocryptine treatment brought about the opposite effect of PRL in almost all parameters studied in both immature and mature monkeys. In general, these findings with prolactin suggests that PRL has a specific and definite influence on testicular neutral lipids and the response of different cellular compartments was found to vary.

Aging↗

PubMed1977

Effect of essential fatty acid deficiency on lipid of skin surface of rat.

A study on how EFA deficiency affects lipid metabolism of rat skin, especially lipid on skin surface, was made. The total amount of lipid on skin surface of rat increased due to EFA deficiency, but not significantly. The sterol ester in skin surface lipid was maintained at a normal level in a EFA deficient rat, but the free sterol level was higher than that of the control rat. The glycerides decreased markedly due to EFA deficiency. It was recognized that branched fatty acids increased in each lipid fraction on skin surface. It was considered that such changes in skin surface lipid were characteristic to skin. It was not predictable whether these changes resulted directly from EFA deficiency or secondary from the occurrence of dermal symptoms.

Animals↗