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PubMedDate not supplied

The effect of hypokinesia on lipid metabolism in adipose tissue.

The increase of nonesterified fatty acid (NEFA) concentration in plasma was observed in rats subjected to hypokinesia for 1-60 days. In the period of recovery (7 and 21 days after 60 days immobilization) the content of NEFA returned to control values. The increase of fatty acid release from adipose tissue was observed in hypokinetic rats, however the stimulation of lipolysis by norepinephrine was lower in rats exposed to hypokinesis. The decrease of the binding capacity and a diminished number of beta-adrenergic receptors were found in animals after hypokinesia. The augmentation of the incorporation of glucose into lipids and the marked increase in the stimulation of lipogenesis by insulin were found in adipose tissue of rats subjected to long-term hypokinesia. These results showed an important effect of hypokinesia on lipid mobilization, on lipogenesis and on the processes of hormone regulation in adipose tissue.

Adipocytes↗
PubMed1988

Control of gluconeogenesis: role of fatty acids in the alpha-adrenergic response.

Phenylephrine increases hepatic gluconeogenesis for as long as it is present in the extracellular medium. This effect is accompanied by a parallel increase in oxygen consumption. No apparent stoichiometric relationship exists between the phenylephrine-stimulated respiration and the energy required to meet the demands of gluconeogenesis. In the absence of extracellular calcium, no sustained stimulation of respiration was observed and phenylephrine failed to enhance gluconeogenesis; however, acute and transient effects of the alpha-adrenergic agonist were still observable. The following observations indicate that fatty acids are not involved in the alpha-adrenergic response: (1) the effects of phenylephrine and octanoate on respiration and gluconeogenesis were found to be additive; (2) unlike phenylephrine, octanoate is capable of stimulating gluconeogenesis in calcium-depleted liver; (3) in the absence of calcium, phenylephrine was incapable of further stimulating respiration or gluconeogenesis in the presence of octanoate. It is concluded that the conditions of increased lipid mobilization and/or oxidation are not sufficient to explain the metabolic response to alpha-adrenergic agonists. Fatty acids and alpha-adrenergic stimulation share a common role of stimulating gluconeogenesis in a manner dependent on their ability to stimulate respiration; however, the additive nature of their effects and distinct calcium requirements indicate that they act to trigger different mechanisms.

Animals↗
PubMed1995

Isolation and primary structures of neuropeptides of the AKH/RPCH family from various termite species.

We have isolated neuropeptides of the AKH/RPCH family from extracts of whole heads of four termite species (Mastotermes darwiniensis, Microhodotermes viator, Hodotermes mossambicus, and Trinervitermes trinervoides) using the effect of mobilizing lipids in Locusta migratoria for bioassay. Isolation was essentially achieved by two steps of reversed-phase chromatography (on phenyl-support followed by C-18). The peptides were identified by Edman degradation after deblocking with oxoprolyl peptidase. Each termite species contained only one AKH/RPCH family member. The primary structure in M. darwiniensis and T. trinervoides is pGlu-Val-Asn-Phe-Ser-Pro-Asn-Trp-NH2, a peptide previously found mainly in cockroaches and code named Pea-CAH-I. The peptide from M. viator has the primary sequence pGlu-Ile-Asn-Phe-Thr-Pro-Asn-Trp-NH2; it is a novel member of the family and is code-named Miv-CC (Microhodotermes viator corpus cardiacum peptide). Phylogenetic relations between the known cockroach and mantid AKH/RPCH octapeptides and the termite peptides from this study could be revealed employing the parsimony method. Based on a computer analysis, using PAUP 3.1.1., we concluded that termites are plesiomorphic with regard to cockroaches, and mantids are the sister taxon to the termite/cockroach group.

Amino Acid Sequence↗
PubMed1987

Blood levels of thyroid hormones and certain metabolites in relation to moult in the harp seal (Phoca groenlandica).

1. Changes in blood levels of thyroxine (T4), triiodothyronine (T3), free fatty acids (FFA), glucose, pyruvic acid and lactic acid in the harp seal during moult, were studied. 2. Serum levels of both T4 and T3 showed significant increase in the moult phase from that in the pre-moult phase. While T4 level continued to remain high during the early and late post-moult phases, T3 level dropped in the latter two phases to the same low pre-moult level. 3. The T3/T4 ratio was significantly higher during the pre-moult phase than that in all the other phases. It is suggested that the high pre-moult T3/T4 ratio marks the initiation of moult. 4. There were no significant changes in the levels of the metabolites studied except that of FFA which was highest in the moult phase indicating the hormonal basis of lipid mobilization.

Animals↗
PubMed1986

Octopamine and cyclic AMP mediate release of adipokinetic hormone I and II from isolated locust neuroendocrine tissue.

Octopamine serves as a neurotransmitter in the glandular lobe of the locust corpus cardiacum where it regulates adipokinetic hormone (AKH) secretion from intrinsic neurosecretory cells. Two AKHs (AKH I and II) from the corpus cardiacum of Locusta have been sequenced and synthesized. We have now demonstrated that octopamine mediates release of both AKH I and II from Locusta corpora cardiaca in vitro. Octopamine, IBMX, and forskolin have previously been shown to elevate levels of cAMP in the glandular lobe. In this paper we demonstrate that IBMX and forskolin mediate secretion of AKH I and AKH II thus mimicking the effects of octopamine in this tissue. The cAMP analogs dibutyryl cAMP and 8-bromo cAMP also elicit release of AKH and a subthreshold concentration of IBMX potentiates the effects of octopamine. These observations demonstrate that cAMP participates in regulating AKH release and support the hypothesis that octopamine mediates hormone release at least in part via changes in intracellular levels of cAMP. The release of AKH I and AKH II is apparently regulated by similar mechanisms. The hyperlipemic activity of AKH II released into the perfusates following stimulation by octopamine and agents which elevate cAMP levels is significantly lower than that of AKH I. This differential response is probably due both to the reduced lipid-mobilizing effect of AKH II relative to AKH I, as well as to the release of greater amounts of AKH I.

Animals↗
PubMed1985

Selectivity in mobilisation of stored fatty acids by maturing cod, Gadus morrhua L.

Lipids, proteins and carbohydrates diminish in the liver and muscle of cod when (a) food is inadequate or (b) the gonads are maturing. The results reported in this paper appear to show that the mobilisation of the lipids differs according to whether the need is just for energy (simple starvation) or for building up gonads. Two groups of fish from the same catch were starved. In one, the gonads were developing, while in the other the gonads had been surgically removed. Significantly more of the fatty acid C22:6 was mobilised from the liver lipids in the group with developing gonads, this fatty acid being present in the greatest amount in the gonads of either sex. The fatty acid C18:1 is also important in the gonads, and this was also preferentially removed from all the livers of maturing-starving fish when compared with gonadectomised-starving, though here the effect was not statistically significant. Some discrimination therefore appears to be exercised when hepatic lipids are removed for gonad development. No selectivity was observed in the mobilisation of fatty acids from the muscle.

Aging↗
PubMed1993

Intracranial tuberculomas: MRI signal intensity correlation with histopathology and localised proton spectroscopy.

In seven cases of intracranial tuberculomas showing different signal intensities on MRI (five characteristic and two nonspecific), detailed histopathological examination was performed to look for number of macrophages, fibrosis, gliosis, degree of inflammatory cellular infiltrate, and type of caseation. The granulomas showing more macrophages, fibrosis and gliosis appeared hypointense on T2-weighted images. Tuberculomas showing minimal macrophages, marked cellular infiltration, and minimal fibrosis appeared hyperintense on T2-weighted images. Lesions showing similar signal intensity on T2-weighted images showed variation in the amount of macrophages, cellular infiltrates, maturity and fibrosis. Trace element estimation was done (iron, copper, and magnesium) in two of these lesions appearing hypointense on T2 and two normal brain samples; these were significantly lower in tuberculoma compared to normal brain tissue. Localised proton spectroscopy was performed in two hypointense lesions which showed marked increase in peaks in the region of mobile lipids (1.28 ppm) compared to normal brain parenchyma. It is concluded that the signal intensity of the lesions is dependent on the number of macrophages, fibrosis and cellular infiltrates. In addition increased lipid contents in the tuberculoma also contribute to the hypointensity on T2-weighted images.

Adult↗
PubMed1996

Inhibition of lipolysis and muscle protein degradation by EPA in cancer cachexia.

Depletion of muscle and adipose tissue in cancer cachexia appears to arise not only from decreased food intake but also from the production of catabolic factors by certain tumours. Experiments with the cachexia-inducing MAC16 tumour in mice showed that when part of the carbohydrate calories were replaced by fish oil, host body weight loss was inhibited. The effect occurred without an alteration of either the total calorie consumption or nitrogen intake. Instead, one of the polyunsaturated fatty acids (PUFA) in fish oil, eicosapentaenoic acid (EPA), was found directly to inhibit tumour-induced lipolysis. The effect was structurally specific, as two related PUFA, docosahexaenoic acid (DHA) and gamma-linolenic acid (GLA), were without effect. The antilipolytic effect of EPA arose from an inhibition of the elevation of cyclic AMP in adipocytes in response to the lipid mobilizing factor. The increased protein degradation in the skeletal muscle of cachectic animals was also inhibited by EPA. This effect was due to the inhibition of the rise in muscle prostaglandin E2 in response to a tumour-produced proteolytic factor by EPA. Thus, reversal of cachexia by EPA in this mouse model results from its capacity to interfere with tumour-produced catabolic factors. Similar factors have been detected in human cancer cachexia.

Adenocarcinoma↗
PubMed2004

Induction of lipolysis in vitro and loss of body fat in vivo by zinc-alpha2-glycoprotein.

Loss of adipose tissue in cancer cachexia has been associated with tumour production of a lipid-mobilizing factor (LMF) which has been shown to be homologous with the plasma protein zinc-alpha(2)-glycoprotein (ZAG). The aim of this study was to compare the ability of human ZAG with LMF to stimulate lipolysis in vitro and induce loss of body fat in vivo, and to determine the mechanisms involved. ZAG was purified from human plasma using a combination of Q Sepharose and Superdex 75 chromatography, and was shown to stimulate glycerol release from isolated murine epididymal adipocytes in a dose-dependent manner. The effect was enhanced by the cyclic AMP phosphodiesterase inhibitor Ro20-1724, and attenuated by freeze/thawing and the specific beta3-adrenoreceptor antagonist SR59230A. In vivo ZAG caused highly significant, time-dependent, decreases in body weight without a reduction in food and water intake. Body composition analysis showed that loss of body weight could be attributed entirely to the loss of body fat. Loss of adipose tissue may have been due to the lipolytic effect of ZAG coupled with an increase in energy expenditure, since there was a dose-dependent increase in expression of uncoupling protein-1 (UCP-1) in brown adipose tissue. These results suggest that ZAG may be effective in the treatment of obesity.

Adipocytes↗
PubMed2003

Red pigment-concentrating hormone is not limited to crustaceans.

A peptide that was previously assumed to occur exclusively in crustaceans is found in the corpora cardiaca of the stinkbug, Nezara viridula. The sequence of the peptide was deduced from the multiple MS(N) electrospray mass data as that of an octapeptide: pGlu-Ile/Leu-Asn-Phe-Ser-Pro-Gly-Trp amide. This peptide with Leu at position 2 is known as crustacean red pigment-concentrating hormone and code-named Panbo-RPCH. The ambiguity about the amino acid at position 2, Leu or Ile, was solved by isolating the peptide in a single-step by reversed-phase HPLC and establishing co-elution with authentic Panbo-RPCH but not with the Ile(2)-analog. When injected into stinkbugs, synthetic Panbo-RPCH elicited an increase of lipids in the haemolymph. Thus, it is assumed that Panbo-RPCH functions in the stinkbug as a lipid-mobilizing hormone.

Animals↗
PubMed2006

Tyramine in the assessment of regional adrenergic function.

Regional adrenergic function is difficult to assess in humans. Tyramine given through a microdialysis probe may be a useful tool in this regard. However, tyramine data is hard to interpret given the drug's complex mode of action. We characterized the response to tyramine, isoproterenol, and dopamine in adipose tissue with microdialysis probes in normal subjects. We measured glycerol concentrations to follow changes in lipolysis and monitored tissue perfusion with ethanol dilution. During perfusion with tyramine, dialysate glycerol concentration increased dose-dependently from 83+/-8 microM at baseline to 181+/-18 microM at 3.5 mM tyramine (p<0.001) followed by a fall down to 121+/-9 microM at 35 mM tyramine (p<0.001). Propranolol almost completely blocked this response. A similar lipolytic response was not observed in isolated human adipocytes. Dopamine <35 microM did not replicate the tyramine-induced lipolysis; however, dopamine >35 microM potently inhibited lipolysis. We conclude that tyramine-induced lipolysis is explained by a pre-synaptic mechanism. Tyramine applied through a microdialysis probe in concentrations up to 3.5 mM can be used to assess pre- and post-synaptic mechanisms regulating lipid mobilization.

Adipocytes↗
PubMed2007

The clinical value of proton magnetic resonance spectroscopy in adult brain tumours.

Proton magnetic resonance spectroscopy (1H MRS) non-invasively provides information on the biochemical profile (typically including up to nine metabolites and mobile lipids) of brain tissue, which varies according to the underlying disease process. A number of studies have assessed its accuracy in the diagnosis of adult brain tumours. This article describes the basic principles of 1H MRS, the metabolic profiles of different brain tumours, and practical points to aid interpretation of spectra. The literature is reviewed regarding the role of 1H MRS in the diagnosis of brain tumours and more specifically where it has proven to be of additional benefit over conventional magnetic resonance imaging.

Adult↗
PubMed2004

Increased juvenile hormone levels after long-duration flight in the grasshopper, Melanoplus sanguinipes.

Although, in many insects, migration imposes a cost in terms of timing or amount of reproduction, in the migratory grasshopper Melanoplus sanguinipes performance of long-duration flight to voluntary cessation or exhaustion accelerates the onset of first reproduction and enhances reproductive success over the entire lifetime of the insect. Since juvenile hormone (JH) is involved in the control of reproduction in most species, we examined JH titer after long flight using a chiral selective radioimmunoassay. JH levels increased on days 5 and 8 in animals flown to exhaustion on day 4 but not in 1-h or non-flier controls. No difference was seen in the diel pattern of JH titer, but hemolymph samples were taken between 5 and 7 h after lights on. Treatment of grasshoppers with JH-III mimicked the effect of long-duration flight in the induction of early reproduction. The increased JH titer induced by performance of long-duration flight is thus at least one component of flight-enhanced reproduction. To test the possibility that post-flight JH titer increases are caused by adipokinetic hormone (AKH) released during long flights, a series of injections of physiological doses of Lom-AKH I were given to unflown animals to simulate AKH release during long flight. This treatment had no effect on JH titers. Thus, although AKH is released during flight and controls lipid mobilization, it is not the factor responsible for increased JH titers after long-duration flight.

Analysis of Variance↗
PubMed2006

Oleoyl-estrone treatment activates apoptotic mechanisms in white adipose tissue.

To determine whether lipid mobilization in white adipose tissue caused by oleoyl-estrone (OE) treatment leads to activation of apoptosis, female Wistar rats were given a daily oral gavage of 10 micromol/kg of OE in 0.2 ml of sunflower oil and DNA fragmentation in different adipose tissues was assessed by ligation-mediated PCR after 6, 24, 48, or 240 h. Expression of selected apoptotic target genes was analysed by RT-PCR in adipose tissue from animals treated for 2 days. The response of adipose tissue to OE treatment was not the same in all locations. In mesenteric adipose tissue, a significant increase in the expression of Bid, Bax, caspase 3 and caspase 8 was detected, whereas in periovaric adipose tissue, only Bax and caspase 3 expression showed significant increases. No effect was detected in subcutaneous or retroperitoneal adipose tissue. The increased expression of apoptotic factors suggests that this pathway could be activated by OE treatment.

Adipose Tissue, White↗
PubMed2006

Nitric oxide production from rat adipocytes is modulated by beta3-adrenergic receptor agonists and is involved in a cyclic AMP-dependent lipolysis in adipocytes.

It is established that the modulation of beta(3)-adrenoceptor function could be associated with impairment of lipolysis in white fat and be responsible for disturbed lipid metabolism. Though two isoforms of nitric oxide synthase (NOS) were reported in adipocytes, the role of nitric oxide (NO) in adipose tissue is still ambiguous. The present work was directed to study the interplay between NO production and beta-adrenoceptor/cyclic AMP (cAMP) pathway on lipid mobilization (glycerol and nonesterified fatty acids, NEFA) in cultures of rat adipocytes isolated from epididymal white adipose tissue. beta-Nonselective (isoprenaline) and beta(3)-selective (BRL-37344) agonists and the postadrenoceptor agents such as dibutyryl-cAMP, forskolin, and 3-isobutyl-1-methylxanthine significantly increased nitrite, glycerol, and NEFA levels with BRL-37344 being the most potent. Conversely, addition of beta-nonselective (propranolol) or beta(3)-selective (bupranolol) antagonist or the adenylyl cyclase inhibitor (SQ 22,536) significantly reduced beta-agonist-induced NO production and lipolysis. For beta-adrenoceptor agonists, antagonists, and their pairs, there was a positive correlation between medium nitrite and glycerol or NEFA with r(2) being 0.90 and 0.84, respectively. The possible relationship between NO and lipolysis was revealed after adipocyte treatment with nonspecific (N(omega)-nitro-l-arginine methyl ester, l-NAME) and specific (aminoguanidine) NOS inhibitors. Both l-NAME and aminoguanidine significantly inhibited the lipolytic effect of BRL-37344. Moreover, NO-donor (S-nitroso-N-acetylpenicillamine) at higher concentration increased basal glycerol and NEFA levels. 8-bromo-cyclic GMP had no effect on adipocyte lipolysis. These data suggest that beta-adrenergic lipolysis, specifically beta(3)-adrenoceptor effect, which is realized via the adenylyl cyclase/cAMP/protein kinase A signaling cascade, involves NO production downstream of beta(3)-adrenoceptor/cAMP pathway.

1-Methyl-3-isobutylxanthine↗
PubMed2005

The effects of neurotensin on selected parameters of lipid metabolism in rats.

15 nM/kg b.m. of neurotensin (NT) caused a significant inhibition of LMA within 30 min of administration and this effect persisted up for to the 240 th minute of the experiment. A 15 nM/kgb.m. dose also caused a reduction in SLA which persisted up to the 120 th minute. Sixty minutes after an intraperitoneal administration of NT a decrease in the cholesterol and NEFA levels and an increase in the TG and glycerol levels were observed. These effects were inhibited by the NTR2-blocker (levocabastine) and were not subject to change after an in vivo application of SR 48692.

Animals↗