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Acute and long-term effects of MDMA on cerebral dopamine biochemistry and function.

RATIONALE AND OBJECTIVES: The majority of experimental and clinical studies on the pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) tend to focus on its action on 5-HT biochemistry and function. However, there is considerable evidence for MDMA having marked acute effects on dopamine release. Furthermore, while MDMA produces long-term effects on 5-HT neurones in most species examined, in mice its long-term effects appear to be restricted to the dopamine system. The objective of this review is to examine the actions of MDMA on dopamine biochemistry and function in mice, rats, guinea pigs, monkeys and humans. RESULTS AND DISCUSSION: MDMA appears to produce a major release of dopamine from its nerve endings in all species investigated. This release plays a significant role in the expression of many of the behaviours that occur, including behavioural changes, alterations of the mental state in humans and the potentially life-threatening hyperthermia that can occur. While MDMA appears to be a selective 5-HT neurotoxin in most species examined (rats, guinea pigs and primates), it is a selective dopamine neurotoxin in mice. Selectivity may be a consequence of what neurotoxic metabolites are produced (which may depend on dosing schedules), their selectivity for monoamine nerve endings, or the endogenous free radical trapping ability of specific nerve endings, or both. We suggest more focus be made on the actions of MDMA on dopamine neurochemistry and function to provide a better understanding of the acute and long-term consequences of using this popular recreational drug.

Animals↗

Cardiac physiology, biochemistry and morphology in response to excess growth hormone in the rat.

The cardiac effects of excess growth hormone (GH) were studied in the intact adult rat and in tissues prepared from the rat. Female Wistar-Furth rats were inoculated with a clonal cell line of pituitary cells which secrete GH. Five weeks later, heart weight had increased 37% compared to control (P less than 0.01) due to concomitant increases in left and right ventricular weight. Hemodynamic measurements in the anesthetized rat showed that GH stimulated rats had a decrease in blood pressure and heart rate and a small increase of left ventricular end-diastolic pressure (P less than 0.05). Measurement of left ventricular contractility and relaxation, and response to beta-adrenergic stimulation were decreased in GH compared to control (P less than 0.05). Contractile protein biochemistry showed an 18% reduction in Ca2(+)-myosin ATPase activity of the left ventricle (P less than 0.05) and non-denaturing pyrophosphate gels of purified myosin demonstrated a significant shift of isoforms from the exclusive V1 pattern to both V1 and V3 isomyosins in both ventricles (P less than 0.05). In contrast to the physiological and protein biochemistry adaptations, left ventricular morphology by light microscopy and ultrastructure by electron microscopy were normal in the GH stimulated heart. There were no significant changes in myofibril fraction, in the myofibril to mitochondria ratio or in the capillary numerical density of the hypertrophied left ventricle (P = N.S.). This study demonstrates that under prolonged and extreme stimulation by GH, the heart undergoes considerable growth/hypertrophy. Although cardiac morphology remains normal during this growth, there are alterations of the isomyosins such that ATPase activity is diminished and ventricular function is decreased.

Animals↗

Metabolism and biochemistry in hypogravity.

The headward shift of body fluid and increase in stress-related hormones that occur in hypogravity bring about a number of changes in metabolism and biochemistry of the human body. Such alterations may have important effects on health during flight and during a recovery period after return to Earth. Body fluid and electrolytes are lost, and blood levels of several hormones that control metabolism are altered during space flight. Increased serum calcium may lead to an increased risk of renal stone formation during flight, and altered drug metabolism could influence the efficacy of therapeutic agents. Orthostatic intolerance and an increased risk of fracturing weakened bones are concerns at landing. It is important to understand biochemistry and metabolism in hypogravity so that clinically important developments can be anticipated and prevented or ameliorated.

Bed Rest↗

Applications of magnetic resonance spectroscopy and diffusion-weighted imaging to the study of brain biochemistry and pathology.

The first practical demonstration that nuclear magnetic resonance (NMR) spectroscopy could be applied to the study of brain biochemistry in vivo came in 1980, with the studies of the rat brain using a surface coil. Since then the technique has been rapidly and extensively developed into a versatile, non-invasive tool for the investigation of various aspects of brain biochemistry, physiology and disease. NMR is non-destructive and can be used to examine a wide variety of samples, ranging from localized regions within the whole brain in humans or animals, through tissue preparations (perfused organ, tissue slices and homogenates), to isolated cells and aqueous solutions, such as tissue extracts. 31P and 1H NMR spectra deriving from endogenous compounds of the brain in situ allow assessment of tissue metabolites and provide information about high-energy phosphates, lactate, certain amino acids, intracellular pH and ionic concentrations. Exogenous substrates or probes labelled with stable isotopes can also be introduced into the brain and used to monitor metabolism. Animal models of brain diseases have given some impetus to rapid progress in clinical NMR spectroscopy and also magnetic imaging techniques. The purpose of this article is to highlight the type of information available from these NMR techniques, and to present this in a neuroscience context, emphasizing the biochemical, physiological and pathological information that can be obtained using these methods.

Animals↗

A retrospective study of the clinical hematology and the serum biochemistry tests made on canine dirofilariasis cases in an animal hospital population in Bangkok, Thailand.

Heartworm disease, caused by the filarial nematode, Dirofilaria immitis, is a major, potentially life-threatening disease of dogs, with worldwide distribution and global significance. It is not only of veterinary importance but it also has zoonotic potential in many regions. It is considered as an endemic disease in Thailand, although clinical data about the disease is rarely reported. The objectives of this study were to characterize the clinical hematology and the biochemistry of canine dirofilariasis cases admitted to Chulalongkorn University, Small Animal Teaching Hospital in Bangkok, Thailand, from 2001-2003. All hematology and serum biochemistry parameter interpretations were based on reference values. A total of 1023 dogs were evaluated in this study. Dogs were divided into three groups based on their heartworm classification (microfilaremic, occult and negative). The major hematological findings in microfilaremic dogs were a mild to moderate anemia, mild to severe thrombocytopenia, marked leukocytosis, moderate to marked neutrophilia, eosinophilia and monocytosis. The most common serum biochemical abnormalities in microfilaremic dogs included increased alkaline phosphatase, alanine aminotransferase and aspartate aminotransferase with a mean+/-SD of 311+/-299, 82+/-76 and 50+/-38 IU/L, respectively. It is likely that this parasitic infection led to the impairment of the hematological and biochemical status of the infected dogs. We believe that investigation of these laboratory based parameters, when associated with the clinical signs, is a very important approach to be considered in the routine clinical follow up, as well as being important for therapeutic evaluations.

Animals↗

Effects of housing, parturition and diet change on the biochemistry and biomechanics of the support structures of the hoof of dairy heifers.

This study investigated effects of housing, diet and parturition on the biochemistry, biomechanics and pathology of feet of maiden, pregnant and lactating dairy heifers. Strength/laxity, laminar morphology, connective tissue (CT) biochemistry and sole lesions were assessed. Although no animals became clinically lame, severity of sole lesions was significantly greater in heifers housed in cubicles vs. straw yards, and in lactating/pregnant heifers vs. maidens. These effects were additive. Cubicle housing and parturition each increased CT metabolism (and were additive), and altered CT composition. Similarly, both impaired the biomechanical resilience of the hoof. There were no effects for diet. The results indicate that parturition/lactation causes non-inflammatory changes in CT that impair resilience of the feet to external stresses associated with poor housing. This "parturition effect" appears to be unrelated to change in diet and relatively brief, unless exacerbated by additional stresses of housing. Thus heifer lameness may be significantly reduced through short-term, low-cost improvements in husbandry around the time of calving.

Animal Feed↗

Combinatorial biochemistry in plants: the case of O-methyltransferases.

Combinatorial chemistry is common place today in chemical synthesis. Virtually thousands of derivatives of a molecule can be achieved by automated systems. The use of biological systems to exploit combinatorial chemistry (combinatorial biochemistry) now has multiple examples in the polyketide field. The modular functional domain structure of polyketide synthases have been recombined through genetic engineering into unnatural constellations in heterologous hosts in order to produce polyketide structures not yet discovered in nature. We present herein an example for a potential type of combinatorial biochemistry in alkaloidal systems using various combinations of Thalictrum tuberosum (meadow rue) O-methyltransferase subunits that result in heterodimeric enzymes with substrate specificities that differ from those of the homodimeric native enzymes.

Combinatorial Chemistry Techniques↗

Kinetic and end-point microdensitometry (section biochemistry) of gamma-glutamyl transpeptidase and dipeptidyl peptidase IV in the mature mouse decidua and visceral yolk sac.

gamma-Glutamyl transpeptidase (EC 2.3.2.2) and dipeptidyl peptidase IV (EC 3.4.14.5) were measured in mature mouse decidual and visceral yolk sac epithelial cells by means of kinetic (continuous) and end-point (static) microdensitometry (section biochemistry). For continuous measurements a new device for starting the enzyme reaction allowed the first readings to be made already during its very early phase. Since the initial reaction rates of both peptidases were very different in the plasma membrane of decidual and also in the visceral yolk sac epithelial cells, it was difficult to select a sufficient number of cells of the same activity for representative measurements on the basis of kinetic microdensitometry. Static section biochemistry was performed also for statistical reasons, i.e., in order to obtain information about the distribution of the activities of the decidual and visceral epithelial cells and the number of measurements required to guarantee valid data. Various groups of decidual and visceral yolk sac epithelial cells with different gamma-glutamyl transpeptidase and dipeptidyl peptidase IV activities were formed. In this way, different activities of gamma-glutamyl transpeptidase were measured in the plasma membrane of the cells of the antimesometrial, intermediate, and mesometrial decidua. Compared with dipeptidyl peptidase IV, gamma-glutamyl transpeptidase was significantly more active in the plasma membrane of the antimesometrial decidual cells and microvillous zone of the visceral yolk sac epithelial cells.

Animals↗

Immunology and biochemistry of Hymenolepis diminuta.

This review is an account of modern research into the immunology and biochemistry of the rat tapeworm, Hymenolepis diminuta. The first half of the review is devoted to the immunological responses of the host to the parasite. It describes the specific responses that occur when the host is exposed to a primary infection, and the changes that occur when further infections are superimposed on the primary one. The aquisition of immunity to the tapeworm and its persistence in the absence of the infection are also discussed, as well as the non-specific responses of the host to the parasite. The second half of the review is concerned with biochemistry, summarizing the early biochemical work that has been carried out on the tapeworm and describing the metabolic pathways now thought to be characteristic of the parasite. What little information that exists on intermediary metabolism in eggs and larvae is summarized here. Much of this section is concerned with the role of mitochondria in H. diminuta, especially the control of the critical branchpoint (PK/PEPCK), which partitions carbon into either the cytosol or the mitochondrion. The role of 5-hydroxytryptamine in controlling both worm behaviour and metabolism is discussed, followed by a brief look at some other effectors that may prove in the future to have great significance in regulating the parasite. Finally, there is a detailed consideration of strain variation within H. diminuta and of the impact on the tapeworm of components of the immune system, formerly described as the 'crowding effect'. The review concludes with a brief discussion of evolutionary aspects of the rat-tapeworm relationship and a comprehensive bibliography.

Animals↗

Pinniped diving response mechanism and evolution: a window on the paradigm of comparative biochemistry and physiology.

Starting even before the end of World War II, the discipline of comparative physiology and biochemistry experienced a period of unprecedented growth and development that pioneers in this field thought would never end. However, by the mid-1970s many of the major mechanistic problems in the field were pretty well understood in principle, and by the mid-1980s workers in the field widely recognized that the discipline was at the point of diminishing returns. One response to this was disillusionment, which turned out to be premature because the field was already absorbing molecular biology tools which has now caused a kind of renaissance in mechanistic physiology studies. The second major response to the sense of disillusionment led to a search for new approaches, and out of this endeavor the newly rejuvenated field of evolutionary physiology arose, and this research area too is now in a growth phase. These general patterns of growth and development in our discipline as a whole are particularly clearly evident in the field of aquatic mammals and birds. Between the 1930s and the 1970s, studies of diving physiology and biochemistry made great progress in mechanistically explaining the basic diving response of aquatic mammals and birds. Key components of the diving response (apnea, bradycardia, peripheral vasoconstriction, redistribution of cardiac output) were found in essentially all species analyzed and were generally taken to be biological adaptations. By the mid-1970s, this approach to unraveling the diving response had run 'out of steam' and was in conceptual stasis. The breakthrough which gave renewal to the field at this time was the development of microprocessor based monitoring of diving animals in their natural environments, which led to a flurry of studies mostly confirming the essential outlines of the diving response based upon laboratory studies and firmly placing it into a proper biological context, underlining its plasticity and species specificities. Now as we begin a new millenium, despite ever more detailed field monitoring of physiology, behavior and ecology, studies aimed at improving understanding of physiological mechanisms in diving are again approaching a point of diminishing returns. To avoid another conceptual stasis, what seems required are new initiatives which may arise from two differing approaches. The first is purely experimental, relying on magnetic resonance imaging (MRI) and spectroscopy (MRS) to expand the framework of the original 'diving response' concept. The second, evolutionary study of the diving response, is synthetic, linked to both field and laboratory studies. To date the evolution of the diving response has only been analyzed in pinnipeds and from these studies two kinds of patterns have emerged. (1) Some physiological and biochemical characters, required and used in diving animals, are highly conserved not only in pinnipeds but in all vertebrates; these traits are necessarily similar in all pinnipeds and include diving apnea, bradycardia, tissue specific hypoperfusion, and hypometabolism of hypoperfused tissues. (2) Another group of functionally linked characters are more malleable and include (i) spleen mass, (ii) blood volume, and (iii) hemoglobin (Hb) pool size. Increases in any of these traits (or in a morphological character, body size) improve diving capacity. Assuming that conserved physiological function means conserved sequences in specific genes and their products (and that evolving function requires changes in such sequences), it is possible to rationalize both the above trait categories in pinniped phylogeny. However, it is more difficult for molecular evolution theory to explain how complex regulatory systems like those involved in bradycardia and peripheral vasoconstriction remain the same through phylogenetic time than it is to explain physiological change driven by directional natural selection.

Animals↗

Xenopus oocytes and the biochemistry of cell division.

The control of cell proliferation involves both regulatory events initiated at the plasma membrane that control reentry into the cell cycle and intracellular biochemical changes that direct the process of cell division itself. Both of these aspects of cell growth control can be studied in Xenopus oocytes undergoing meiotic maturation in response to mitogenic stimulation. All mitogenic signaling pathways so far identified lead to the phosphorylation of ribosomal protein S6 on serine residues, and the biochemistry of this event has been investigated. Insulin and other mitogens activate ribosomal protein S6 kinase II, which has been cloned and sequences in oocytes and other cells. This enzyme is activated by phosphorylation on serine and threonine residues by an insulin-stimulated protein kinase known as MAP-2 kinase. MAP kinase itself is also activated by direct phosphorylation on threonine and tyrosine residues in vivo. These results reconstitute one step of the insulin signaling pathway evident shortly after insulin receptor binding at the membrane. Several hours after mitogenic stimulation, a cell cycle cytoplasmic control element is activated that is sufficient to cause entry into M phase. This control element, known as maturation-promoting factor or MPF, has been purified to near homogeneity and shown to consist of a complex between p34cdc2 protein kinase and cyclin B2. In addition to apparent phosphorylation of cyclin, regulation of MPF activity involves synthesis of the cyclin subunit and its periodic degradation at the metaphase----anaphase transition. The p34cdc2 kinase subunit is regulated by phosphorylation/dephosphorylation on threonine and tyrosine residues, being inactive when phosphorylated and active when dephosphorylated. Analysis of phosphorylation sides in histone H1 for p34cdc2 has revealed a consensus sequence of (K/R)S/TP(X)K/R, where the elements in parentheses are present in some but not all sites. Sites with such a consensus are specifically phosphorylated in mitosis and by MPF in the protooncogene pp60c-src. These results provide a link between cell cycle control and cell growth control and suggest that changes in cell adhesion and the cytoskeleton in mitosis may be regulated indirectly by MPF via protooncogene activation. S6 kinase II is also activated upon expression of MPF in cells, indicating that MPF is upstream of S6 kinase on the mitogenic signaling pathway. Further study both of the signaling events that lead to MPF activation and of the substrates for phosphorylation by MPF should lead to a comprehensive understanding of the biochemistry of cell division.

Animals↗

Effect of long-term dietary supplementation of high-gamma-linolenic canola oil versus borage oil on growth, hematology, serum biochemistry, and N-6 fatty acid metabolism in rats.

Dietary supplementation of a high-gamma-linolenic acid canola oil (HGCO) containing approximately 36% (w/w) of gamma-linolenic acid (GLA, 18:3n-6) from the seeds of a genetically transformed canola strain, was assessed for its long-term biological effects. Growing Sprague-Dawley rats (n = 30) were fed a purified AIN93G diet containing 5, 10, or 15% (w/w) of HGCO as the fat source. For comparison, a separate group of rats (n = 10) was given the diet containing 15% (w/w) of borage oil (BO), which contained 22% (w/w) of GLA. After 12 weeks of feeding, the growth, relative organ weights, hematology, and serum biochemistry were found to be similar among rats fed the 5, 10, and 15% HGCO diets. The GLA levels in plasma and liver phospholipids (PL) were also similar. However, the levels of GLA in peripheral tissues (muscle PL and adipose triacylglycerols) were significantly higher in rats fed the 10 and 15% HGCO diets than those fed the 5% HGCO diet. When the above biologic parameters were compared between the 15% HGCO and 15% BO dietary groups, there were no significant differences except for lower final body weights and higher tissue levels of GLA, dihomo-gamma-linolenic acid (20:3n-6) and arachidonic acid (20:4n-6) in the 15% HGCO dietary group as compared with the 15% BO dietary group. This is due to a higher GLA content and possibly a more favorable stereospecific distribution of GLA in HGCO. Overall, long-term (12-week) feeding with diets containing up to 15% HGCO resulted in no adverse effects on growth, organ weight, hematology and serum biochemistry as compared to the diet containing 15% BO, suggesting that HGCO may be a safe alternative source of GLA.

Adipose Tissue↗

Clinical pharmacokinetics of epirubicin: the importance of liver biochemistry tests.

The influence of liver biochemistry tests on epirubicin pharmacokinetics has been investigated in 52 women with advanced breast cancer, 27 of whom had radiologically proven liver metastases. Patients received epirubicin 12.5-120 mg m-2 given as an i.v. bolus. Epirubicin levels were measured by HPLC following the first cycle of treatment. Epirubicin elimination, expressed as clearance (dose/AUC), in the 22 patients with normal AST and bilirubin was compared with that of 30 patients with a raised AST +/- raised bilirubin. Epirubicin clearance was significantly reduced in the patients with a raised AST, whether their serum bilirubin was normal (22 patients) or elevated (eight patients). In the 30 patients with a raised AST +/- raised bilirubin, epirubicin clearance correlated strongly with the level of AST (r = -0.72) but not with serum bilirubin, alkaline phosphatase, albumin or creatinine. Using a multiple regression analysis, AST was the only one of these biochemical variables predictive of epirubicin clearance (r2 = 0.47, P = 0.0006). We conclude that a raised serum AST is a more sensitive and reliable measure of abnormal epirubicin pharmacokinetics than increased bilirubin. These findings have implications for anthracycline treatment in patients with abnormal liver biochemistry.

Adult↗

Expression of epidermal-growth-factor receptor in the K562 cell line by transfection. Altered receptor biochemistry.

The epidermal-growth-factor (EGF) receptor was expressed in the human erythroleukaemic cell line K562 by transfection of the receptor cDNA. EGF-receptor biochemistry appears altered in the K562 transfectants. Autophosphorylation of the K562 receptor is not stimulated substantially by EGF. Tyrosine kinase activity of the receptor is high in the absence of EGF, whereas receptor affinity for EGF is low. K562 cells are shown to lack mRNA for transforming growth factor alpha (TGF alpha). Therefore autocrine stimulation of the K562 receptor, at least by TGF alpha, does not explain the observed receptor biochemistry. The K562 receptor is phosphorylated at a single major site in intact cells, a threonine residue that may be Thr-669. Possible mechanisms of regulation of the EGF receptor in the K562 transfectants are discussed.

DNA↗

Effect of environmental haemin upon the physiology and biochemistry of Prevotella intermedia R78.

The effect of environmental haemin on the physiology and biochemistry of Prevotella intermedia R78 grown in batch culture was assessed. Extent and rate of growth increased as the environmental haemin concentration was raised. In addition, cell morphology was predominantly cocco-bacillary when cultured in high haemin environments, while bacillary forms were prevalent in low haemin conditions (< 2.5 mumol l-1). Cells harvested from low haemin environments produced greater numbers of extracellular vesicles and greater amounts of peptidolytic activity, haemagglutinating potential and haemin binding activity when compared with cells harvested from high haemin conditions. The results of the present study indicate that aspects of the biochemistry and physiology of P. intermedia are influenced by changes in environmental haemin levels.

Culture Media↗

First-trimester screening for fetal aneuploidy: biochemistry and nuchal translucency.

Maternal dried whole-blood specimens were collected prospectively from 2010 singleton pregnancies between 9 + 0 and 13 + 4 weeks that included 18 chromosomally abnormal pregnancies (11 Down's syndrome, four trisomy 18, two trisomy 13 and one triploidy). A subset of 744 pregnancies underwent ultrasound nuchal translucency measurement and included seven Down's syndrome, four trisomy 18, two trisomy 13 and one triploidy. Patients were evaluated for risk of Down's syndrome and trisomy 18 based on biochemistry (free beta-human chorionic gonadotropin and pregnancy-associated plasma protein A), nuchal translucency and the combination of both. In prospective biochemical screening, false-positive rates for Down's syndrome and trisomy 18 were 5.1% (66/1297) and 1.9% (25/1297) in women < 35 years of age and 14.2% (99/695) and 1.6% (11/695) in women > or = 35 years of age, respectively. The detection efficiency of aneuploidy was 6/6 (100%) in women < 35 years and 11/12 (92%) in women > or = 35 years. Nuchal translucency measurement alone detected 57% (8/14) of cases of aneuploidy at a 5.8% (42/730) false-positive rate. Modelling with the age distribution of live births, a 5% false-positive rate resulted in Down's syndrome detection efficiency of 61% by biochemistry, 73% by nuchal translucency and 87% by combining both methods. The data in this study demonstrate that combined biochemical and ultrasound evaluation for Down's syndrome and other chromosomal abnormalities in the first trimester of pregnancy yield a detection capability that may exceed that of current second-trimester prenatal screening protocols. The potential for enhanced detection coupled to an earlier alert of fetal complications could represent a substantial advantage to both clinician and patient.

Adolescent↗

Selenium redox biochemistry of zinc-sulfur coordination sites in proteins and enzymes.

Selenium has been increasingly recognized as an essential element in biology and medicine. Its biochemistry resembles that of sulfur, yet differs from it by virtue of both redox potentials and stabilities of its oxidation states. Selenium can substitute for the more ubiquitous sulfur of cysteine and as such plays an important role in more than a dozen selenoproteins. We have chosen to examine zinc-sulfur centers as possible targets of selenium redox biochemistry. Selenium compounds release zinc from zinc/thiolate-coordination environments, thereby affecting the cellular thiol redox state and the distribution of zinc and likely of other metal ions. Aromatic selenium compounds are excellent spectroscopic probes of the otherwise relatively unstable functional selenium groups. Zinc-coordinated thiolates, e.g., metallothionein (MT), and uncoordinated thiolates, e.g., glutathione, react with benzeneseleninic acid (oxidation state +2), benzeneselenenyl chloride (oxidation state 0) and selenocystamine (oxidation state -1). Benzeneseleninic acid and benzeneselenenyl chloride react very rapidly with MT and titrate substoichiometrically and with a 1:1 stoichiometry, respectively. Selenium compounds also catalyze the release of zinc from MT in peroxidation and thiol/disulfide-interchange reactions. The selenoenzyme glutathione peroxidase catalytically oxidizes MT and releases zinc in the presence of t-butyl hydroperoxide, suggesting that this type of redox chemistry may be employed in biology for the control of metal metabolism. Moreover, selenium compounds are likely targets for zinc/thiolate coordination centers in vivo, because the reactions are only partially suppressed by excess glutathione. This specificity and the potential to undergo catalytic reactions at low concentrations suggests that zinc release is a significant aspect of the therapeutic antioxidant actions of selenium compounds in antiinflammatory and anticarcinogenic agents.

Animals↗

Recent advances in the nutritional biochemistry of trivalent chromium.

The nutritional biochemistry of trivalent Cr has been a poorly understood field of study; investigations of the biochemistry of the other essential transition metals have not proven as problematic. Despite over four decades of endeavour, only recently has a picture of the role of Cr potentially started to be defined. The biologically-relevant form is the trivalent ion. Cr3+ appears to be required for proper carbohydrate and lipid metabolism in mammals, although fortunately Cr deficiency is difficult to achieve. Conditions that increase circulating glucose and insulin concentrations increase urinary Cr output. Cr is probably excreted in the form of the oligopeptide chromodulin. Chromodulin may be the key to understanding the role of Cr at a molecular level, as the molecule has been found to bind to activated insulin receptor, stimulating its kinase activity. A mechanism for the action of chromodulin has recently been proposed; this mechanism can serve as a potential framework for further studies to test the role of Cr in metabolism. An examination of the nutritional supplement chromium picolinate illustrates some of the difficulties associated with these biochemical studies.

Animals↗