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PubMed2004

Insulin increases the abundance of the growth hormone receptor in liver and adipose tissue of periparturient dairy cows.

After parturition, increased growth hormone (GH) secretion is important to preserve the metabolic homeostasis of energy-deficient dairy cows. Elevated plasma GH promotes lipid mobilization from adipose tissue, but paradoxically, is associated with depressed concentration of insulin-like growth factor-I (IGF-I), a growth factor produced in a GH-dependent fashion in liver. Primary factors regulating GH responses of liver and adipose tissue are poorly understood in periparturient dairy cows. Consistent with insulin being such a factor, its plasma concentration declined concomitantly with net energy balance (EB) and with plasma IGF-I in a group of 9 periparturient dairy cows. To test the role of insulin in regulating cellular determinants of GH responsiveness, hyperinsulinemic-euglycemic clamps were performed on 6 dairy cows in late pregnancy (28 d prepartum) before the reductions in EB, insulin, and IGF-I were initiated, and when they were completed in early lactation (10 d postpartum). Infusion of insulin nearly doubled the plasma concentration of IGF-I (P < 0.001) and hepatic levels of IGF-I mRNA during both states (P < 0.05). In liver, these responses were associated with increased abundance of the GH receptor protein (GHR; P < 0.05), whereas the abundance of intracellular mediators of GH actions (JAK2, STAT5, or STAT3) remained unaffected. Insulin also doubled GHR abundance in adipose tissue (P < 0.01), indicating that this effect is not liver specific. These results raise the possibility that insulin regulates the efficiency of GH signaling in liver and adipose tissue of dairy cows by acting as a rheostat of GHR synthesis.

Adipose Tissue↗
PubMed2000

Quantification of microheterogeneity in glioblastoma multiforme with ex vivo high-resolution magic-angle spinning (HRMAS) proton magnetic resonance spectroscopy.

Microheterogeneity is a routinely observed neuropathologic characteristic in brain tumor pathology. Although microheterogeneity is readily documented by routine histologic techniques, these techniques only measure tumor status at the time of biopsy or surgery and do not indicate likely tumor progression. A biochemical screening technique calibrated against pathologic standards would greatly assist in predicting tumor progression from its biological activity. Here we demonstrate for the first time that proton magnetic resonance spectroscopy (1H MRS) with high-resolution magic-angle spinning (HRMAS), a technique introduced in 1997, can preserve tissue histopathologic features while producing well-resolved spectra of cellular metabolites in the identical intact tissue specimens. Observed biochemical alterations and tumor histopathologic characteristics can thus be correlated for the same surgical specimen, obviating the problems caused by tumor microheterogeneity. We analyzed multiple specimens of a single human glioblastoma multiforme surgically removed from a 44-year-old patient. Each specimen was first measured with HRMAS 1H MRS to determine tumor metabolites, then evaluated by quantitative histopathology. The concentrations of lactate and mobile lipids measured with HRMAS linearly reflected the percentage of tumor necrosis. Moreover, metabolic ratios of phosphorylcholine to choline correlated linearly with the percentage of the highly cellular malignant glioma. The quantification of tumor metabolic changes with HRMAS 1H MRS, in conjunction with subsequent histopathology of the same tumor specimen, has the potential to further our knowledge of the biochemistry of tumor heterogeneity during development, and thus ultimately to improve our accuracy in diagnosing, characterizing, and evaluating tumor progression.

Adult↗
PubMed1996

Chronic ethanol consumption ameliorates the maturity-onset diabetes-obesity syndrome in CBA mice.

The effects of a chronic ethanol drinking schedule (20% solution for 6 weeks) on energy balance and carbohydrate and lipid metabolism have been investigated in lean (32-36 g) and obese-diabetic (40-44 g) CBA/Ca mice. The untreated obese-diabetic mice exhibited hyperglycaemia, hypertriglyceridaemia, hyper-insulinaemia and insulin resistance. The chronic ethanol treatment, which yielded plasma ethanol levels of between 1 and 11 mM, lowered the blood glucose, plasma insulin and triacylglycerol levels towards normal in the obese mice, but did not affect these parameters in the lean mice. The body weight of the obese mice tended to return to normal during the 6-week drinking period, although their total energy intake (9.2-10.0 kJ/g/week, food plus ethanol-derived calories) was almost double that of the lean mice (4.8-5.4 kJ/g/week). The blood glucose response to acute insulin injection, which was significantly reduced in the obese mice, became indistinguishable from the response of normal mice after chronic ethanol treatment. Soleus muscle glycogen synthesis in both lean and obese mice was not significantly altered by ethanol drinking, but brown adipose tissue lipogenesis was significantly increased (by 50%) in the obese mice. It is proposed that ethanol is acting chronically to restore insulin sensitivity in the obese diabetic mice at doses which have little or no effect in normal lean animals. This action is exerted, at least in part, at the level of brown adipose tissue lipogenesis.

Adipose Tissue, Brown↗
PubMed1993

Cancer cachexia.

Cachexia is a common problem in the clinical management of cancer patients, particularly those with solid tumors. Cachexia is most obviously manifested as weight loss with massive depletion of both adipose tissue and muscle mass, and death is probably due to loss of lean body tissue. Not only is the survival time shorter in patients with cachexia, but the frequency of response to chemotherapy is also significantly reduced. Although anorexia frequently accompanies cachexia, attempts to halt or reverse cachexia by nutritional repletion have not been successful. This suggests that cachexia is due to metabolic abnormalities produced by the tumor in addition to the underlying anorexia. In some patients weight loss is associated with an increased relative energy expenditure possibly through an elevated adrenergic state. Several factors have been postulated as mediators of cancer cachexia and can be divided into two groups. (i) Materials with hormone-like characteristics which result in direct catabolism of host tissues. (ii) Cytokines which cause alterations in host metabolism indirectly. Included in group (i) are the conventional catabolic hormones and a lipid mobilizing factor (LMF) produced by tumors, which causes direct breakdown of adipose tissue. Included in group (ii) are tumor necrosis factor-alpha, interleukin-6, interferon-gamma and leukaemia inhibitory factor. The materials appear to influence adipose tissue indirectly through an inhibition of lipoprotein lipase. Reversal of cachexia has been achieved by two groups of agents. (i) Those stimulating food intake, e.g. megestrol acetate. (ii) Those directly inhibiting the LMF, e.g. eicosapentaenoic acid. While agents in group (i) can cause tumor growth stimulation, those in group (ii) act as tumor growth inhibitors. This latter results suggests that the products of catabolism of host tissues may be important for tumor growth and provides a new avenue for chemotherapeutic intervention.

Animals↗
PubMedDate not supplied

Proton NMR spectroscopy of cerebral metabolic alterations in infantile peroxisomal disorders.

Noninvasive studies of cerebral metabolism were performed with use of localized proton MR spectroscopy (MRS) in both healthy controls (n = 4, age 6 weeks to 2 years) and infants (n = 4, age 3-15 months) who had impaired peroxisomal functions classified as variants of Zellweger syndrome. All patients revealed a marked decrease of N-acetylaspartate in white and gray matter, thalamus, and cerebellum, indicating impairment of normal neuronal development as well as neuronal loss. In two cases an increase of cerebral glutamine and a decrease of the cytosolic polyol myo-inositol in gray matter and striatum reflected the impact of a concomitant effect on hepatic function. Two cases 3 and 6 months of age exhibited a notable elevation of mobile lipids and/or cholesterol in white matter. These patients with severe disease died within 4 weeks after the MRS examination. While an increase of free fatty acids generally associated with a lysosomal storage disease was not consistently observed by proton MRS of brain, this technique provides a convenient and safe tool for the direct assessment of neuropathologic aspects of Zellweger syndrome such as neuronal degeneration, demyelination, and consequences of compromised liver function.

Adrenoleukodystrophy↗
PubMedDate not supplied

Serial proton magnetic resonance spectroscopy in lesions of Balò concentric sclerosis.

OBJECTIVE: Balò concentric sclerosis is a rare demyelinating disorder. Serial proton magnetic resonance spectroscopic (1H-MRS) studies were carried out to better understand the biochemical changes within concentric lesions. MATERIALS AND METHODS: Five concentric lesions in four patients with Balò concentric sclerosis were chosen as the objects of serial observation. They included two early acute lesions (showing as concentric ring enhancement on magnetic resonance imaging (MRI) after gadolinium administration), two late acute lesions (showing as marginal enhancement on MRI), and one early subacute lesion (showing as edematous concentric lesions without enhancement on MRI). The duration of follow-up ranged from 2-23 months (mean 10 months). A total of 20 1H-MRS studies were performed. On each 1H-MRS study, short-echo (30 ms) and long-echo (136 ms) spectra were obtained. The peaks of N-acetyl-asparate (NAA), choline-containing compounds (Cho), creatine and phosphocreatine (Cr), lactate, and mobile lipid were observed and compared. RESULTS: Generally, a decrease of NAA/Cr ratio and an increase of Cho/Cr ratio were seen on all the spectra. Observing longitudinally, a trend of decreasing NAA/Cr ratio first and then partially recovering later was noted. The lowest level of NAA/Cr ratio was noted at the late acute stage or early subacute stage. The Cho/Cr ratio and amplitude of the lactate peak showed a similar trend as that of NAA/Cr, but in an opposite direction. It was rising first and descending later. The highest levels of Cho/Cr ratio and lactate peak were also observed at the late acute or early subacute stage. In addition, lactate peaks could be detected as long as 7 months after onset of symptoms. Lipid metabolite (two broad peaks at 0.9-1.5 ppm) was seen at the initial study of each group, but fluctuated in size on follow-up. CONCLUSION: The characteristic biochemical changes of concentric sclerosis were a decreased NAA/Cr ratio, an increased Cho/Cr ratio, two broad peaks at 0.9-1.5 ppm, lactate production, and a reversible NAA/Cr ratio on follow-up. The serial 1H-MRS studies revealed a strong biochemical association between NAA, Cho, and lactate, which may be caused by the same pathogenetic process of demyelination and inflammatory cellular infiltration. The specificity of the serial changes may provide information about the stage of the concentric lesion and perhaps aid in monitoring progression of concentric lesions and evaluating therapy.

Adult↗
PubMed2006

Pharmacological approaches to ameliorating catabolic conditions.

PURPOSE OF REVIEW: Nutritional debilitation is among the most devastating and life-threatening aspect of various diseases. It arises from a complex interaction between the illness and the host. This process includes cytokine production, release of lipid-mobilizing and proteolysis-inducing factors, and alterations in intermediary metabolism. As a result, many patients develop cachexia with progressive body fat and muscle tissue wasting with associated worsening of their clinical status and a lower quality of life. In this review, up-to-date information about different approaches to pharmacologic management of cachexia will be addressed. RECENT FINDINGS: Until recently, the two major options for pharmacological therapy were either progestational agents or corticosteroids. Knowledge of the mechanisms of cachexia, however, has led to newer therapeutic interventions for treating several aspects of the syndrome. These include antiserotonergic agents, branched-chain amino acids, eicosapentaenoic acid, cannabinoids, melatonin, and thalidomide--all of which act on the feeding-regulatory circuitry to increase appetite and inhibit illness-derived catabolic factors. SUMMARY: Information from this review will guide health care providers in limiting weight loss and improving performance status of cachectic patients through pharmacological therapy, with the hope that such therapy will extend patients' survival and improve their qualities of life.

Adrenal Cortex Hormones↗
PubMed1975

The dynamic properties of biological membranes.

Biological membranes must be viewed as highly dynamic, undergoing continuous structural fluctuations and changes in response to external perturbations. The study of liposomes by 31 P n.m.r. and fluorescence can reveal some of the motional characteristics of the different regions in a bilayer. Asymmetric lipid distribution and how this depends on the environment is also observed by n.m.r. The nature of the interaction of amine anaesthetics and of polypeptide antibodies with membranes is discussed in relation to their perturbing effect. The role of lipid mobility in modulating hormone-receptor interaction is discussed with reference to the binding of thyroid stimulating hormone.

4-Aminobenzoic Acid↗
PubMed1999

Characterization of tissue damage in multiple sclerosis by nuclear magnetic resonance.

Nuclear magnetic resonance (NMR) imaging is an established diagnostic medium to diagnose multiple sclerosis (MS). In clinically stable MS patients, NMR detects silent disease activity, which is the reason why it is being used to monitor treatment trials, in which it serves as a secondary outcome parameter. The absence of a clear correlation with clinical disability, the so-called 'clinico-radiological' paradox, and the poor predictive value of NMR prohibit the use of NMR as a primary outcome parameter in clinical trials. This is--among others--a result of the limited histopathological specificity of conventional, or 'T2-weighted' imaging, the most commonly used NMR technique. In this paper we review additional NMR techniques with higher tissue specificity, most of which show marked heterogeneity within NMR-visible lesions, reflecting histopathological heterogeneity. Gadolinium enhancement identifies the early inflammatory phase of lesion development, with active phagocytosis by macrophages. Persistently hypointense lesions on T1-weighted images ('black holes') relate to axonal loss and matrix destruction, and show a better correlation with clinical disability. Marked prolongation of T1 relaxation time correlates with enlargement of the extracellular space, which occurs as a result of axonal loss or oedema. Axonal viability can also be measured using the concentration of N-acetyl aspartate (NAA) using NMR spectroscopy; this technique is also capable of showing lactate and mobile lipids in lesions with active macrophages. The multi-exponential behaviour of T2 relaxation time in brain white matter provides a tool to monitor the myelin water component in MS lesions (short T2 component) as well as the expansion of the extracellular space (long T2 component). Chemical exchange with macromolecules (e.g. myelin) can be measured using magnetization transfer imaging, and correlates with demyelination, axonal loss and matrix destruction. Increased water diffusion has been found in MS lesions (relating to oedema and an expanded extracellular space) and a loss of anisotropy may indicate a loss of fibre orientation (compatible with demyelination). Apart from the histopathological heterogeneity within focal MS lesions, the normal-appearing white matter shows definite abnormalities with all quantifiable NMR techniques. A decrease in the concentration of NAA, decreased magnetization transfer values and prolonged T1 relaxation time values are probably all related to microscopic abnormalities, including axonal damage. This 'invisible' lesion load may constitute a significant proportion of the total lesion load but is not visible on conventional NMR. Similarly, mechanisms for clinical recovery exist, which are not distinguished using MR imaging. Therefore, it is highly unlikely that the clinico-radiological paradox will ever be solved completely. However, NMR provides an opportunity to sequentially measure tissue changes in vivo. Using MR parameters with (presumed) histopathological specificity, the development of (irreversible) tissue damage can be monitored, which perhaps allows the identification of factors that determine lesional outcome in MS. Since the absence of severe tissue destruction is prognostically favourable, NMR monitoring of the extent to which such changes can be prevented by treatment will ultimately benefit the selection of future treatment strategies.

Blood-Brain Barrier↗
PubMed1988

A comparative spin-label study of isolated plasma membranes and plasma membranes of whole cells and protoplasts from cold-hardened and nonhardened winter rye.

Lipid-lipid and lipid-protein interactions in the plasma membranes of whole cells and protoplasts and an isolated plasma membrane fraction from winter rye (Secale cereale L. cv Puma) have been studied by spin labeling. Spectra were recorded between -40 degrees C and 40 degrees C using the freely diffusing spin-label, 16-doxyl stearic acid, as a midbilayer membrane probe. The probe was reduced by the whole cells and protoplasts and reoxidized by external potassium ferricyanide. The reoxidized probe was assumed to be localized in the plasma membrane. The spectra consisted of the superposition of a narrow and a broad component indicating that both fluid and immobilized lipids were present in the plasma membrane. The two components were separated by digital subtraction of the immobilized component. Temperature profiles of the membranes were developed using the percentage of immobilized lipid present at each temperature and the separation between the outermost hyperfine lines for the fluid lipid component. Lipid immobilization was attributed to lipid-protein interactions, lipid-cell wall interactions, and temperature-induced lipid phase transitions to the gel-state. Temperature profiles were compared for both cold-hardened and nonhardened protoplasts, plasma membranes, and plasma membrane lipids, respectively. Although cold-hardening extended the range of lipid fluidity by 5 degrees C, it had no effect on lipid-protein interactions or activation energies of lipid mobility. Differences were found, however, between the temperature profiles for the different samples, suggesting that alterations in the plasma membrane occurred as a consequence of the isolation methods used.

Journal Article↗
PubMed2004

Peroxisomal Acyl-CoA synthetase activity is essential for seedling development in Arabidopsis thaliana.

In plants and other eukaryotes, long-chain acyl-CoAs are assumed to be imported into peroxisomes for beta-oxidation by an ATP binding cassette (ABC) transporter. However, two genes in Arabidopsis thaliana, LACS6 and LACS7, encode peroxisomal long-chain acyl-CoA synthetase (LACS) isozymes. To investigate the biochemical and biological roles of peroxisomal LACS, we identified T-DNA knockout mutants for both genes. The single-mutant lines, lacs6-1 and lacs7-1, were indistinguishable from the wild type in germination, growth, and reproductive development. By contrast, the lacs6-1 lacs7-1 double mutant was specifically defective in seed lipid mobilization and required exogenous sucrose for seedling establishment. This phenotype is similar to the A. thaliana pxa1 mutants deficient in the peroxisomal ABC transporter and other mutants deficient in beta-oxidation. Our results demonstrate that peroxisomal LACS activity and the PXA1 transporter are essential for early seedling growth. The peroxisomal LACS activity would be necessary if the PXA1 transporter delivered unesterified fatty acids into the peroxisomal matrix. Alternatively, PXA1 and LACS6/LACS7 may act in parallel pathways that are both required to ensure adequate delivery of acyl-CoA substrates for beta-oxidation and successful seedling establishment.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1989

Coordinate expression of transcriptionally regulated isocitrate lyase and malate synthase genes in Brassica napus L.

We have analyzed the temporal and spatial expression of genes encoding the glycoxylate cycle enzymes isocitrate lyase and malate synthase in Brassica napus L. to determine whether they are coordinately expressed. Both enzymes participate in reactions associated with lipid mobilization in oilseed plant seedlings and are sequestered in a specialized organelle, the glyoxysome. We have identified an isocitrate lyase cDNA clone containing the complete protein coding region. RNA blot and in situ hybridization studies with isocitrate lyase and malate synthase cDNA clones from B. napus showed that the genes exhibit similar expression patterns. The mRNAs begin to accumulate during late embryogeny, reach maximal levels in seedling cotyledons, are not detected at significant amounts in leaves, and are distributed similarly in cotyledons and axes of seedlings. Furthermore, transcription studies with isolated nuclei indicate that the genes are controlled primarily although not exclusively at the transcriptional level. We conclude that glyoxysome biogenesis is regulated in part through the coordinate expression of isocitrate lyase and malate synthase genes.

Amino Acid Sequence↗
PubMed1975

The effect of norepinephrine and theophylline on blood glucose, plasms FFA, plasma glycerol and plasma insulin in normal subjects.

The plasma concentrations of free fatty acids (FFA), glycerol and insulin as well as the blood glucose concentration have been followed in two groups of subjects after infusions of theophyllamine. Each individual was examined twice. The 5 subjects in group 2 were given an infusion of norepinephrine before the theophyllamine at one of the examinations and saline at the other. The 6 subjects in group II were given an infusion of norephinephrine at both examinations, followed by theophyllamine on one occasion and by saline on the other. Thus, the subjects in both groups served as their own controls. It was found that theophyllamine caused lipid mobilization, as measured by the plasma FFA and plasma glycerol concentrations, both when given as the only active drug and when given after norepinephrine. The blood glucose concentration rose slightly after norepinephrine and the plasma insulin level increased concomittantly. When theophylline was given as the only active drug, there was no increase in the blood glucose but the plasma insulin concentration rose slightly.

Adult↗
PubMed1985

Long-term beta 1-selective adrenergic blockade and adrenergic receptors in human subcutaneous adipocytes.

The influence of beta-adrenergic blockade with metoprolol, a beta 1-selective agent, on the adrenergic regulation of lipid mobilization was explored in subcutaneous adipocytes removed from 13 patients with essential hypertension. Treatment with metoprolol, which was associated with adequate beta-adrenergic blockade and an antihypertensive effect, resulted in a significant increase (p less than 0.05) in the binding of the beta-adrenergic antagonist (-)-(3H)-dihydroalprenolol and a 50% increase (p less than 0.01) in the maximum lipolytic response to the beta-adrenergic agonist isopropylnoradrenaline. In 7 patients with normotriglyceridaemia the total plasma triglyceride level increased significantly (p less than 0.025) during metoprolol treatment, a change that was due to an increase in the very low density lipoprotein triglycerides. The findings suggest that chronic treatment with the beta 1-selective adrenergic blocker metoprolol leads to a significant increase in beta-adrenoceptor density and an increase in the lipolytic response to beta-adrenergic agonists. This latter finding may, in some measure, account for the increased plasma triglyceride level observed.

Adipose Tissue↗
PubMed1984

Influence of fasting on lipolytic response to adrenergic agonists and on adrenergic receptors in subcutaneous adipocytes.

The influence of 1 week's total fasting on the lipolytic effect of adrenergic agonists and on the binding of adrenergic antagonists was examined in isolated adipocytes of subcutaneous specimens removed from the hypogastric and the femoral sites in seventeen obese women. In the femoral adipocytes the lipolytic sensitivity to isopropyl noradrenaline decreased 30-fold (P less than 0.01) during fasting. The specific binding of the radioligands (-)-[3H]-dihydroalprenolol and (-)-[125I]-cyanopindolol decreased significantly during fasting, essentially owing to a reduction in the receptor density. In adipocytes from the hypogastric region no such changes were found. For both tissue regions fasting induced a right-ward shift in the dose-response curve for the inhibitory effect of the alpha 2 agonist, clonidine, on theophylline-induced lipolysis, corresponding to a 10-fold decrease in sensitivity. There was also a significant decrease of about 20% in the alpha 2-adrenoceptor density, as estimated with the radioligand [3H]-yohimbine. The results suggest that the regulation of the lipid mobilization in man by the sympathetic nervous system during fasting occurs not only through an increase in the level of circulating noradrenaline but also through changes in the adrenergic receptor density of the adipocytes.

Adipose Tissue↗
PubMed1987

Role of alpha-adrenoceptors for adipocyte size in man.

Catecholamines have dual effects on lipid mobilization in man. Lipolysis is stimulated via beta-adrenoceptors and inhibited via alpha 2-adrenoceptors. The relationship between fat-cell size and catecholamine-induced lipolysis (expressed per cell surface area) was investigated in vitro in subcutaneous adipocytes of thirty-five non-obese subjects between 1 month and 45 years of age. Fat-cell volume showed a positive correlation with noradrenaline-induced lipolysis (r = 0.7). Furthermore, fat-cell size showed a negative correlation with the alpha 2-effect of noradrenaline (r = 0.8) but no correlation with the beta-effect of the hormone (r less than 0.1). Although age showed a positive correlation with noradrenaline-induced rate of lipolysis (r = 0.6) it did not contribute to the relationship between cell size and the catecholamine effect. There was no relationship between adipocyte size and the basal (unstimulated) rate of lipolysis (r less than 0.1). In conclusion, ageing in non-obese subjects is associated with enlargement of fat-cell size and enhancement of the lipolytic effect of catecholamines. The latter is due to diminished alpha 2-anti-lipolytic effect of the hormones. This modulation of the alpha 2-adrenoceptor activity may be of importance for the regulation of adipocyte size in man.

Adipose Tissue↗
PubMed2004

Pathogenicity of Stagonospora nodorum requires malate synthase.

A gene encoding malate synthase, a key enzyme of the glyoxylate cycle, has been cloned and characterized in the necrotrophic wheat pathogen Stagonospora nodorum. Expression studies of Mls1 showed high levels of transcript in ungerminated spores whereas malate synthase enzyme activities were low. Expression studies in planta found that Mls1 transcript levels decreased approximately 10-fold upon germination before slowly increasing throughout the remainder of the infection. To characterize Mls1 further, the gene was disrupted in S. nodorum by homologous recombination. In the absence of any supplied carbon source, the mls1 spores were unable to germinate and consequently the mutants were non-pathogenic. Germination and pathogenicity could be restored by the addition of either glucose or sucrose, implying that S. nodorum is reliant upon the catabolism of lipids for infection. Furthermore, analysis of lipid bodies in the mutant strain indicated that lipid mobilization and, consequently, peroxisomal beta-oxidation of fatty acids is delayed or inhibited by the disruption of the glyoxylate cycle. This study has demonstrated for the first time in a fungal phytopathogen the requirement of malate synthase for pathogenicity, suggesting that gluconeogenesis is both dependent on the glyoxylate cycle and required for infection.

Ascomycota↗