ABSTRACT
El Código Alimentario Argentino establece: "Con la denomi-nación de leche sin calificativo alguno, se entiende el producto obtenido por el ordeño total e ininterrumpido, en condiciones de higiene, de la vaca lechera en buen estado de salud y ali-mentación, proveniente de tambos inscriptos y habilitados por la Autoridad Sanitaria Bromatológica Jurisdiccional y sin aditivos de ninguna especie"1. La leche de vaca es un componente cuantitativamente útil en la alimentación humana en gran parte debido al acceso generali-zado a partir de su industrialización y comercialización. Su com-posición la hace de interés para adaptar su uso y prescripción en distintos momentos de la vida y en la promoción de la salud.Según estudios de investigación, los efectos no se limitarían exclu-sivamente a su valor nutricional, sino que sumarían otros poten-ciales en determinadas patologías como la enfermedad cardiovas-cular, algunos tipos de cáncer, hipertensión arterial, en patología ósea o dental y en la lucha frente al sobrepeso y la obesidad.Por este motivo, el Grupo de Trabajo Alimentos de la Sociedad Argentina de Nutrición realizó esta revisión sobre los potenciales efectos de la leche: virtuosos o adversos.
Subject(s)
Humans , Milk , Nutritive Value , Peptides/physiology , Calcium/physiology , Milk/adverse effectsABSTRACT
BACKGROUND: A link between diabetes and Parkinson´s disease (PD) has been established by several reports. Consistent data report that people diagnosed with diabetes have demonstrated an enhanced risk of manifesting PD in their lifetime. The working principles involved in this link have been extensively discussed. Over the last decade, diabetes has been reported to be correlated with an increased risk of dementia, suggesting a potential role of diabetes, or insulin signalling dysregulations, in neurodegeneration. In addition, it is nowadays highly debated that dysregulations related to Ca2+ signalling may be an upstream issue which could also link diabetes and PD. Ca2+ and cAMP signalling pathways (Ca2+/cAMP signalling) control both the neurotransmitters/hormones release and neuronal death. CONCLUSION: Considering our previous reports about Ca2+/cAMP signalling, the putative contribution of Ca2+/cAMP signalling in this link (between diabetes and PD) is discussed in this paper.
Subject(s)
Calcium/physiology , Cyclic AMP/physiology , Diabetes Mellitus/physiopathology , Parkinson Disease/physiopathology , Signal Transduction/physiology , Humans , Parkinson Disease/etiologyABSTRACT
Intrathecal (i.t.) administration of quinpirole, a dopamine (DA) D2-like receptor agonist, produces antinociception to mechanonociceptive stimuli but not to thermonociceptive stimuli. To determine a cellular mechanism for the specific antinociceptive effect of D2-like receptor activation on mechanonociception, we evaluated the effect of quinpirole on voltage-gated Ca2+ influx in cultured dorsal root ganglion (DRG) neurons and the D2 DA receptor distribution in subpopulations of rat nociceptive DRG neurons. Small-diameter DRG neurons were classified into IB4+ (nonpeptidergic) and IB4- (peptidergic). Intracellular [Ca2+] microfluorometry and voltage-clamp experiments showed that quinpirole reduced Ca2+ influx and inhibited the high voltage-activated Ca2+ current (HVA-ICa) in half of IB4+ neurons, leaving Ca2+ entry and HVA-ICa in IB4- neurons nearly unaffected. Pretreatment with ω-conotoxin MVIIA prevented the effect of quinpirole on HVA-ICa from IB4+ neurons, indicating that quinpirole mainly inhibits CaV2.2 channels. Immunofluorescence experiments showed that D2 DA receptor was present mainly in IB4+ small DRG neurons. Finally, in behavioral experiments in rats, the clinically approved D2-like receptor agonist pramipexole produced spinal antinociception in a similar fashion to quinpirole, with a significant effect only in the mechanonociceptive test. Our results explain, at least in part, why D2-like receptor agonists produce antinociception on mechanonociceptors.
Subject(s)
Nociception/drug effects , Nociception/physiology , Receptors, Dopamine D2/metabolism , Spinal Cord/drug effects , Spinal Cord/physiology , 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine/pharmacology , Animals , Calcium/metabolism , Calcium/physiology , Dopamine Agonists/pharmacology , Ganglia, Spinal/drug effects , Ganglia, Spinal/metabolism , Ganglia, Spinal/physiology , Male , Nociceptors/drug effects , Nociceptors/metabolism , Nociceptors/physiology , Pramipexole/pharmacology , Quinpirole/pharmacology , Rats , Rats, Wistar , Spinal Cord/metabolismABSTRACT
Trypanosomatids are a group of flagellated unicellular eukaryotes, causing serious human diseases including Chagas disease (Trypanosoma cruzi), sleeping sickness (Trypanosoma brucei spp.) and Leishmaniasis (Leishmania spp.). The second messenger cAMP is involved in numerous and fundamental processes in these parasites including differentiation between stages, proliferation, osmoregulation, oxidative stress and quorum sensing. Interestingly, its signaling pathway is quite different from that of mammals, including structurally different adenylyl cyclases, the shortage of orthologous effector proteins and the absence of G-protein-coupled-receptors, among others. These characteristics make the proteins involved in these transduction pathways good candidates for therapeutic targets. However, the identification of new unknown druggable targets involves extensive research time and is economically very expensive, making difficult the transition from basic research to the clinical phase. Trypanosomatid PDEs have characteristic binding pockets that allow for a differential inhibition from their human orthologs. Modification in the approved drugs for human to convert them into trypanocidal treatments could lead to more effective therapies, shorter lab time and lower costs. In view of the fact that kinetoplastid PDEs are highly conserved with their mammalian counterparts, and since there are already numerous drugs on the market against human PDEs, the drug repositioning approach is highly promising. The development of new technologies, higher government and industrial involvement and more scientists committed to basic investigation, are the key to ultimately find an effective treatment and cure for the neglected tropical diseases.
Subject(s)
Phosphodiesterase Inhibitors/pharmacology , Signal Transduction/drug effects , Adenylyl Cyclases/physiology , Calcium/physiology , Chagas Disease/drug therapy , Drug Repositioning , Humans , Leishmania donovani/enzymology , Leishmania donovani/physiology , Protein Kinases/physiology , Trypanosoma brucei brucei/drug effects , Trypanosoma brucei brucei/enzymology , Trypanosoma brucei brucei/physiology , Trypanosoma cruzi/drug effects , Trypanosoma cruzi/enzymology , Trypanosoma cruzi/physiologyABSTRACT
Obesity is often associated with changes in cardiac function; however, the mechanisms responsible for functional abnormalities have not yet been fully clarified. Considering the lack of information regarding high-saturated-fat diet-induced obesity, heart function, and the proteins involved in myocardial calcium (Ca2+) handling, the aim of this study was to test the hypothesis that this dietary model of obesity leads to cardiac dysfunction resulting from alterations in the regulatory proteins of intracellular Ca2+ homeostasis. Male Wistar rats were distributed into two groups: control (C, n=18; standard diet) and obese (Ob, n=19; high-saturated-fat diet), which were fed for 33 weeks. Cardiac structure and function were evaluated using echocardiographic and isolated papillary muscle analyses. Myocardial protein expressions of sarcoplasmic reticulum Ca2+-ATPase, phospholamban (PLB), PLB serine-16 phosphorylation, PLB threonine-17 phosphorylation, ryanodine receptor, calsequestrin, Na+/Ca2+ exchanger, and L-type Ca2+ channel were assessed by western blot. Obese rats presented 104% increase in the adiposity index (C: 4.5±1.4 vs Ob: 9.2±1.5%) and obesity-related comorbidities compared to control rats. The left atrium diameter (C: 5.0±0.4 vs Ob: 5.5±0.5 mm) and posterior wall shortening velocity (C: 36.7±3.4 vs Ob: 41.8±3.8 mm/s) were higher in the obese group than in the control. The papillary muscle function was similar between the groups at baseline and after inotropic and lusitropic maneuvers. Obesity did not lead to changes in myocardial Ca2+ handling proteins expression. In conclusion, the hypothesis was not confirmed, since the high-saturated-fat diet-induced obese rats did not present cardiac dysfunction or impaired intracellular Ca2+ handling proteins.
Subject(s)
Calcium/physiology , Diet, High-Fat/adverse effects , Heart/physiopathology , Obesity/physiopathology , Sodium-Calcium Exchanger/physiology , Animals , Blood Pressure/physiology , Disease Models, Animal , Echocardiography , Male , Rats , Rats, WistarABSTRACT
Obesity is often associated with changes in cardiac function; however, the mechanisms responsible for functional abnormalities have not yet been fully clarified. Considering the lack of information regarding high-saturated-fat diet-induced obesity, heart function, and the proteins involved in myocardial calcium (Ca2+) handling, the aim of this study was to test the hypothesis that this dietary model of obesity leads to cardiac dysfunction resulting from alterations in the regulatory proteins of intracellular Ca2+ homeostasis. Male Wistar rats were distributed into two groups: control (C, n=18; standard diet) and obese (Ob, n=19; high-saturated-fat diet), which were fed for 33 weeks. Cardiac structure and function were evaluated using echocardiographic and isolated papillary muscle analyses. Myocardial protein expressions of sarcoplasmic reticulum Ca2+-ATPase, phospholamban (PLB), PLB serine-16 phosphorylation, PLB threonine-17 phosphorylation, ryanodine receptor, calsequestrin, Na+/Ca2+ exchanger, and L-type Ca2+ channel were assessed by western blot. Obese rats presented 104% increase in the adiposity index (C: 4.5±1.4 vs Ob: 9.2±1.5%) and obesity-related comorbidities compared to control rats. The left atrium diameter (C: 5.0±0.4 vs Ob: 5.5±0.5 mm) and posterior wall shortening velocity (C: 36.7±3.4 vs Ob: 41.8±3.8 mm/s) were higher in the obese group than in the control. The papillary muscle function was similar between the groups at baseline and after inotropic and lusitropic maneuvers. Obesity did not lead to changes in myocardial Ca2+ handling proteins expression. In conclusion, the hypothesis was not confirmed, since the high-saturated-fat diet-induced obese rats did not present cardiac dysfunction or impaired intracellular Ca2+ handling proteins.
Subject(s)
Animals , Male , Rats , Calcium/physiology , Sodium-Calcium Exchanger/physiology , Diet, High-Fat/adverse effects , Heart/physiopathology , Obesity/physiopathology , Blood Pressure/physiology , Echocardiography , Rats, Wistar , Disease Models, AnimalABSTRACT
Ca2+ is essential for proper structure and function of skeletal muscle. It not only activates contraction and force development but also participates in multiple signaling pathways. Low levels of Ca2+ restrain muscle regeneration by limiting the fusion of satellite cells. Ironically, sustained elevations of Ca2+ also result in muscle degeneration as this ion promotes high rates of protein breakdown. Moreover, transforming growth factors (TGFs) which are well known for controlling muscle growth also regulate Ca2+ channels. Thus, therapies focused on changing levels of Ca2+ and TGFs are promising for treating muscle-wasting disorders. Three principal systems govern the homeostasis of Ca2+, namely, excitation-contraction (EC) coupling, excitation-coupled Ca2+ entry (ECCE), and store-operated Ca2+ entry (SOCE). Accordingly, alterations in these systems can lead to weakness and atrophy in many hereditary diseases, such as Brody disease, central core disease (CCD), tubular aggregate myopathy (TAM), myotonic dystrophy type 1 (MD1), oculopharyngeal muscular dystrophy (OPMD), and Duchenne muscular dystrophy (DMD). Here, the interrelationship between all these molecules and processes is reviewed.
Subject(s)
Calcium Signaling , Calcium/physiology , Homeostasis , Muscle, Skeletal/physiopathology , Muscular Atrophy/physiopathology , Excitation Contraction Coupling , Humans , Muscular Diseases/genetics , Muscular Diseases/physiopathologyABSTRACT
Insect and vertebrate hearts share the ability to generate spontaneously their rhythmic electrical activity, which triggers the fluid-propelling mechanical activity. Although insects have been used as models in studies on the impact of genetic alterations on cardiac function, there is surprisingly little information on the generation of the inotropic activity in their hearts. The main goal of this study was to investigate the sources of Ca2+ for contraction in Tenebrio molitor hearts perfused in situ, in which inotropic activity was assessed by the systolic variation of the cardiac luminal diameter. Increasing the pacing rate from 1.0 to 2.5 Hz depressed contraction amplitude and accelerated relaxation. To avoid inotropic interference of variations in spontaneous rate, which have been shown to occur in insect heart during maneuvers that affect Ca2+ cycling, experiments were performed under electrical pacing at near-physiological rates. Raising the extracellular Ca2+ concentration from 0.5 to 8 mM increased contraction amplitude in a manner sensitive to L-type Ca2+ channel blockade by D600. Inotropic depression was observed after treatment with caffeine or thapsigargin, which impair Ca2+ accumulation by the sarcoplasmic reticulum (SR). D600, but not inhibition of the sarcolemmal Na+/Ca2+ exchanger by KB-R7943, further depressed inotropic activity in thapsigargin-treated hearts. From these results, it is possible to conclude that in T. molitor heart, as in vertebrates: (a) inotropic and lusitropic activities are modulated by the heart rate; and (b) Ca2+ availability for contraction depends on both Ca2+ influx via L-type channels and Ca2+ release from the SR.
Subject(s)
Calcium/physiology , Heart/physiology , Myocardial Contraction/physiology , Sarcoplasmic Reticulum/physiology , Tenebrio/physiology , Animals , Calcium Channels, L-Type/physiology , Female , In Vitro Techniques , Insect Proteins/physiology , MaleABSTRACT
Circadian clocks impose daily periodicities to animal behavior and physiology. At their core, circadian rhythms are produced by intracellular transcriptional/translational feedback loops (TTFL). TTFLs may be altered by extracellular signals whose actions are mediated intracellularly by calcium and cAMP. In mammals these messengers act directly on TTFLs via the calcium/cAMP-dependent transcription factor, CREB. In the fruit fly, Drosophila melanogaster, calcium and cAMP also regulate the periodicity of circadian locomotor activity rhythmicity, but whether this is due to direct actions on the TTFLs themselves or are a consequence of changes induced to the complex interrelationship between different classes of central pacemaker neurons is unclear. Here we investigated this question focusing on the peripheral clock housed in the non-neuronal prothoracic gland (PG), which, together with the central pacemaker in the brain, controls the timing of adult emergence. We show that genetic manipulations that increased and decreased the levels of calcium and cAMP in the PG caused, respectively, a shortening and a lengthening of the periodicity of emergence. Importantly, knockdown of CREB in the PG caused an arrhythmic pattern of eclosion. Interestingly, the same manipulations directed at central pacemaker neurons caused arrhythmicity of eclosion and of adult locomotor activity, suggesting a common mechanism. Our results reveal that the calcium and cAMP pathways can alter the functioning of the clock itself. In the PG, these messengers, acting as outputs of the clock or as second messengers for stimuli external to the PG, could also contribute to the circadian gating of adult emergence.
Subject(s)
Calcium/physiology , Circadian Clocks/physiology , Cyclic AMP/physiology , Drosophila melanogaster/physiology , Signal Transduction/genetics , Animals , Brain/physiology , Calcium Channels/genetics , Circadian Rhythm/physiology , Drosophila Proteins/genetics , Drosophila Proteins/metabolism , Endocrine Glands/metabolism , Female , Gene Knockdown Techniques , Locomotion/physiology , Male , Sarcoplasmic Reticulum Calcium-Transporting ATPases/genetics , Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolismABSTRACT
KEY POINTS: We investigated the excitation-contraction coupling mechanisms in small pulmonary veins (SPVs) in rat precision-cut lung slices. We found that SPVs contract strongly and reversibly in response to extracellular ATP and other vasoconstrictors, including angiotensin-II and endothelin-1. ATP-induced vasoconstriction in SPVs was associated with the stimulation of purinergic P2Y2 receptors in vascular smooth muscle cell, activation of phospholipase C-ß and the generation of intracellular Ca2+ oscillations mediated by cyclic Ca2+ release events via the inositol 1,4,5-trisphosphate receptor. Active constriction of SPVs may play an important role in the development of pulmonary hypertension and pulmonary oedema. ABSTRACT: The small pulmonary veins (SPVs) may play a role in the development of pulmonary hypertension and pulmonary oedema via active changes in SPV diameter, mediated by vascular smooth muscle cell (VSMC) contraction. However, the excitation-contraction coupling mechanisms during vasoconstrictor stimulation remain poorly understood in these veins. We used rat precision-cut lung slices and phase-contrast and confocal microscopy to investigate dynamic changes in SPV cross-sectional luminal area and intracellular Ca2+ signalling in their VSMCs. We found that the SPV (â¼150 µm in diameter) contract strongly in response to extracellular ATP and other vasoconstrictors, including angiotensin-II and endothelin-1. ATP-induced SPV contraction was fast, concentration-dependent, completely reversible upon ATP washout, and inhibited by purinergic receptor antagonists suramin and AR-C118925 but not by MRS2179. Immunofluorescence showed purinergic P2Y2 receptors expressed in SPV VSMCs. ATP-induced SPV contraction was inhibited by phospholipase Cß inhibitor U73122 and accompanied by intracellular Ca2+ oscillations in the VSMCs. These Ca2+ oscillations and SPV contraction were inhibited by the inositol 1,4,5-trisphosphate receptor inhibitor 2-APB but not by ryanodine. The results of the present study suggest that ATP-induced vasoconstriction in SPVs is associated with the activation of purinergic P2Y2 receptors in VSMCs and the generation of Ca2+ oscillations.
Subject(s)
Calcium/physiology , Muscle Contraction , Myocytes, Smooth Muscle/physiology , Pulmonary Veins/physiology , Receptors, Purinergic P2Y2/metabolism , Vasoconstriction , Adenosine Triphosphate/metabolism , Animals , Cells, Cultured , Cross-Sectional Studies , Excitation Contraction Coupling , Inositol 1,4,5-Trisphosphate Receptors/metabolism , Myocytes, Smooth Muscle/cytology , Phospholipase C beta/metabolism , Pulmonary Veins/cytology , RatsABSTRACT
Introduction: Hypercalcemia can cause different neurological disorders, depending on the calcium level. We report an exceptional case of primary hyperparathyroidism presenting as neurological alteration and it has favourable outcome after parathyroidectomy. Case report: A 74-year-old woman presented with progressive cognitive deterioration and impaired motor function. The complementary tests showed hypercalcemia due to a parathyroid adenoma. Parathyroidectomy was performed with symptomatic improvement. Conclusion: Cognitive impairment of the elderly due to a parathyroid adenoma is underdiagnosed, behavioral changes and alterations of motor functions are attributed to age, dementia and frailty, representing a diagnostic challenge.
Introducción: La hipercalcemia puede causar diferentes trastornos neurológicos, dependiendo de las concentraciones de calcio. Aportamos un caso excepcional de hiperparatiroidismo primario que se manifestó con deterioro neurológico rápidamente evolutivo y se resolvió mediante paratiroidectomía. Caso clínico: Mujer de 74 años que consultó por deterioro cognitivo progresivo y alteración de las funciones motoras. Las pruebas complementarias evidenciaron hipercalcemia debida a un adenoma paratiroideo. Se realizó paratiroidectomía, con mejoría sintomática. Conclusión: El deterioro cognitivo del anciano por un adenoma paratiroideo está infradiagnosticado, pues los cambios de conducta y las alteraciones de las funciones motoras se atribuyen a la edad, la demencia y la fragilidad, suponiendo un reto diagnóstico.
Subject(s)
Hyperparathyroidism, Primary/complications , Parathyroidectomy , Parkinsonian Disorders/etiology , Adenoma/complications , Adenoma/surgery , Aged , Brain/pathology , Calcium/physiology , Cognition Disorders/etiology , Dementia/diagnosis , Diagnostic Errors , Female , Humans , Hypercalcemia/etiology , Hyperparathyroidism, Primary/surgery , Magnetic Resonance Imaging , Parathyroid Neoplasms/complications , Parathyroid Neoplasms/surgery , Recovery of FunctionABSTRACT
KEY POINTS: Extracellular ATP, in association with [Ca2+ ]i regulation, is required to maintain basal ciliary beat frequency. Increasing extracellular ATP levels increases ciliary beating in airway epithelial cells, maintaining a sustained response by inducing the release of additional ATP. Extracellular ATP levels in the millimolar range, previously associated with pathophysiological conditions of the airway epithelium, produce a transient arrest of ciliary activity. The regulation of ciliary beat frequency is dependent on ATP release by hemichannels (connexin/pannexin) and P2X receptor activation, the blockage of which may even stop ciliary movement. The force exerted by cilia, measured by atomic force microscopy, is reduced following extracellular ATP hydrolysis. This result complements the current understanding of the ciliary beating regulatory mechanism, with special relevance to inflammatory diseases of the airway epithelium that affect mucociliary clearance. ABSTRACT: Extracellular nucleotides, including ATP, are locally released by the airway epithelium and stimulate ciliary activity in a [Ca2+ ]i -dependent manner after mechanical stimulation of ciliated cells. However, it is unclear whether the ATP released is involved in regulating basal ciliary activity and mediating changes in ciliary activity in response to chemical stimulation. In the present study, we evaluated ciliary beat frequency (CBF) and ciliary beating forces in primary cultures from mouse tracheal epithelium, using videomicroscopy and atomic force microscopy (AFM), respectively. Extracellular ATP levels and [Ca2+ ]i were measured by luminometric and fluorimetric assays, respectively. Uptake of ethidium bromide was measured to evaluate hemichannel functionality. We show that hydrolysis of constitutive extracellular ATP levels with apyrase (50 U ml-1 ) reduced basal CBF by 45% and ciliary force by 67%. The apyrase effect on CBF was potentiated by carbenoxolone, a hemichannel inhibitor, and oxidized ATP, an antagonist used to block P2X7 receptors, which reduced basal CBF by 85%. Additionally, increasing extracellular ATP levels (0.1-100 µm) increased CBF, maintaining a sustained response that was suppressed in the presence of carbenoxolone. We also show that high levels of ATP (1 mm), associated with inflammatory conditions, lowered basal CBF by reducing [Ca2+ ]i and hemichannel functionality. In summary, we provide evidence indicating that airway epithelium ATP release is the molecular autocrine mechanism regulating basal ciliary activity and is also the mediator of the ciliary response to chemical stimulation.
Subject(s)
Adenosine Triphosphate/physiology , Cilia/physiology , Epithelial Cells/physiology , Respiratory Mucosa/physiology , Animals , Calcium/physiology , Cells, Cultured , Male , Mice, Inbred BALB C , Respiratory Mucosa/cytology , Trachea/physiologyABSTRACT
Calcium (Ca2+) is a key player in the regulation of many cell functions. Just like Ca2+, mitochondria are ubiquitous, versatile, and dynamic players in determining both cell survival and death decisions. Given their ubiquitous nature, the regulation of both is deeply intertwined, whereby Ca2+ regulates mitochondrial functions, while mitochondria shape Ca2+ dynamics. Deregulation of either Ca2+ or mitochondrial signaling leads to abnormal function, cell damage or even cell death, thereby contributing to muscle dysfunction or cardiac pathologies. Moreover, altered mitochondrial Ca2+ homeostasis has been linked to metabolic diseases like cancer, obesity, and pulmonary hypertension. In this review article, we summarize the mechanisms that coordinate mitochondrial and Ca2+ responses and how they affect human health. © 2017 American Physiological Society. Compr Physiol 7:623-634, 2017.
Subject(s)
Calcium Signaling/physiology , Calcium/metabolism , Mitochondria/physiology , Animals , Calcium/physiology , Cell Death/physiology , Homeostasis/physiology , Humans , Mitochondria/metabolism , Neurodegenerative Diseases/metabolismABSTRACT
In the vertebrate retina, three types of photoreceptors-visual photoreceptor cones and rods and the intrinsically photosensitive retinal ganglion cells (ipRGCs)-converged through evolution to detect light and regulate image- and nonimage-forming activities such as photic entrainment of circadian rhythms, pupillary light reflexes, etc. ipRGCs express the nonvisual photopigment melanopsin (OPN4), encoded by two genes: the Xenopus (Opn4x) and mammalian (Opn4m) orthologs. In the chicken retina, both OPN4 proteins are found in ipRGCs, and Opn4x is also present in retinal horizontal cells (HCs), which connect with visual photoreceptors. Here we investigate the intrinsic photosensitivity and functioning of HCs from primary cultures of embryonic retinas at day 15 by using calcium fluorescent fluo4 imaging, pharmacological inhibitory treatments, and Opn4x knockdown. Results show that HCs are avian photoreceptors with a retinal-based OPN4X photopigment conferring intrinsic photosensitivity. Light responses in HCs appear to be driven through an ancient type of phototransduction cascade similar to that in rhabdomeric photoreceptors involving a G-protein q, the activation of phospholipase C, calcium mobilization, and the release of the inhibitory neurotransmitter GABA. Based on their intrinsic photosensitivity, HCs may have a key dual function in the retina of vertebrates, potentially regulating nonvisual tasks together with their sister cells, ipRGCs, and with visual photoreceptors, modulating lateral interactions and retinal processing.
Subject(s)
Photoreceptor Cells, Vertebrate/physiology , Retinal Horizontal Cells/physiology , Rod Opsins/physiology , Animals , Calcium/physiology , Cells, Cultured , Chickens , Embryo, Nonmammalian , Light , Retinaldehyde/physiology , Rod Opsins/genetics , gamma-Aminobutyric Acid/physiologyABSTRACT
This experiment aimed to evaluate the utilization of firewood ash as calcium source in the initial diet of broiler chickens. One hundred and twenty eight broiler chickens of Cobb-500® strain, from 1 to 21 days of age, were randomly distributed in four treatments with four repetitions of eight birds each, been four female and four male. The experimental diets were corn-soybean based, been isoenergetic and isonutrients, and had 0, 0.32, 0.98 and 1.27% of firewood ash as calcium source. The firewood ash utilized had 23.8% of calcium, 0.39% of total phosphorus, and 0.11% of sodium. The experimental treatments did not influence the feed intake, body weight, body weight gain, and food conversion from 1 to 7, 1 to 14, and 1 to 21 days of age. The tibia and femur thickness and length at 21 days of age were not altered by treatments. It was concluded that the firewood ash can be used as calcium sourcereplacing limestone in the initial diet of broiler chickens, without change the performance and the bone development.
Subject(s)
Animals , Food Additives/analysis , Ash/analysis , Calcium, Dietary/analysis , Calcium/physiology , Eating , Nutrition Programs , Dietary Supplements/analysis , Weight Gain/physiology , Animal Nutritional Physiological Phenomena , Femur/anatomy & histology , Phosphorus, Dietary/analysis , Body Weight/physiology , Glycine max/physiology , Sodium, Dietary/analysis , Tibia/anatomy & histology , Zea mays/physiologyABSTRACT
This experiment aimed to evaluate the utilization of firewood ash as calcium source in the initial diet of broiler chickens. One hundred and twenty eight broiler chickens of Cobb-500® strain, from 1 to 21 days of age, were randomly distributed in four treatments with four repetitions of eight birds each, been four female and four male. The experimental diets were corn-soybean based, been isoenergetic and isonutrients, and had 0, 0.32, 0.98 and 1.27% of firewood ash as calcium source. The firewood ash utilized had 23.8% of calcium, 0.39% of total phosphorus, and 0.11% of sodium. The experimental treatments did not influence the feed intake, body weight, body weight gain, and food conversion from 1 to 7, 1 to 14, and 1 to 21 days of age. The tibia and femur thickness and length at 21 days of age were not altered by treatments. It was concluded that the firewood ash can be used as calcium sourcereplacing limestone in the initial diet of broiler chickens, without change the performance and the bone development.(AU)
Subject(s)
Animals , Ash/analysis , Food Additives/analysis , Calcium, Dietary/analysis , Calcium/physiology , Eating , Dietary Supplements/analysis , Nutrition Programs , Animal Nutritional Physiological Phenomena , Zea mays/physiology , Glycine max/physiology , Phosphorus, Dietary/analysis , Sodium, Dietary/analysis , Weight Gain/physiology , Body Weight/physiology , Tibia/anatomy & histology , Femur/anatomy & histologyABSTRACT
Calcium intake has a role on the development of peak bone mass, and has a mild impact on the maintenance of bone mass during adulthood and the reduction of bone loss rate in postmenopausal women and the elderly in both genders. Calcium dietary intake should be privileged over supplementation. Dairy products are the main calcium dietary sources. Prospective studies have not clearly demonstrated an effect on the prevention of fractures, because of the practical difficulties of a long follow-up in order to get to solid conclusions; however the physiological rationale is that an adequate calcium intake and 25(OH) vitamin D levels exceeding 20 ng/ml is beneficial for bone health and may decrease to certain extent the risk of fractures.
Subject(s)
Calcium, Dietary/administration & dosage , Calcium/physiology , Fractures, Bone/prevention & control , Osteoporosis/prevention & control , Adult , Bone Density , Female , Humans , Male , Prospective Studies , Vitamin D/administration & dosage , Vitamin D/blood , Vitamins/administration & dosageABSTRACT
The P2X7 receptor is a member of the P2X family of ligand-gated ion channels. A single-nucleotide polymorphism leading to a glutamine (Gln) by arginine (Arg) substitution at codon 460 of the purinergic P2X7 receptor (P2X7R) has been associated with mood disorders. No change in function (loss or gain) has been described for this SNP so far. Here we show that although the P2X7R-Gln460Arg variant per se is not compromised in its function, co-expression of wild-type P2X7R with P2X7R-Gln460Arg impairs receptor function with respect to calcium influx, channel currents and intracellular signaling in vitro. Moreover, co-immunoprecipitation and FRET studies show that the P2X7R-Gln460Arg variant physically interacts with P2X7R-WT. Specific silencing of either the normal or polymorphic variant rescues the heterozygous loss of function phenotype and restores normal function. The described loss of function due to co-expression, unique for mutations in the P2RX7 gene so far, explains the mechanism by which the P2X7R-Gln460Arg variant affects the normal function of the channel and may represent a mechanism of action for other mutations.
Subject(s)
Polymorphism, Single Nucleotide/genetics , Receptors, Purinergic P2X7/physiology , Blotting, Western , Calcium/metabolism , Calcium/physiology , Fluorescence Resonance Energy Transfer , HEK293 Cells , Humans , Immunoprecipitation , Patch-Clamp Techniques , Polymorphism, Single Nucleotide/physiology , RNA, Small Interfering/metabolism , Real-Time Polymerase Chain Reaction , Receptors, Purinergic P2X7/genetics , Receptors, Purinergic P2X7/metabolism , Signal Transduction/physiologyABSTRACT
Introdução: A obesidade é considerada importante problema de saúde pública e fator de risco para o desenvolvimento de doenças cardiovasculares. Estudos apontam que o trânsito de cálcio (Ca+2) intracelular e extracelular, mecanismo essencial no acoplamento excitação-contração-relaxamento cardíaco, está envolvido nesse processo patológico. Enquanto o influxo de Ca+2 promove aumento da concentração de Ca+2 livre no citosol na fase de contração, a recaptura e a extrusão do Ca+2 são importantes para a diminuição do Ca+2 intracelular durante o relaxamento. Objetivo: Identificar, baseado na literatura científica, a modulação da disfunção cardíaca pelo trânsito de cálcio em modelos de obesidade genética e dietética. Métodos: A busca de artigos em bases de dados eletrônicas foi realizada com palavras-chaves e seus correspondentes em inglês. Resultados: Inicialmente os artigos que apresentassem uma das palavras-chaves no título foram selecionados. Após processo de triagem, foram identificados 23 artigos para leitura na íntegra. Foram selecionados ao debate na seção "Discussão" apenas 18 artigos, visto que apresentaram conteúdo satisfatório sobre o tema abordado. Conclusão: A literatura mostra que a obesidade, genética ou dietética, promove disfunções cardíacas moduladas por diversas alterações no trânsito de Ca+2 intracelular e em suas proteínas regulatórias.
Introduction: Obesity is considered an important public that presents increasing prevalence on a global scene. Obese individuals have greater susceptibility to the development of cardiac disease. Studies show that calcium (Ca2+) handling, essential mechanism in the process contraction-relaxation of the cardiac muscle, is associated with cardiac dysfunction in obesity models. While Ca2+ influx promotes elevation of free Ca2 + concentration in the cytosol in the contraction period, the recapture and extrusion Ca2 + are important to Ca2+ reduction during the relaxation. Objective: To identify, based on scientific literature, modulation of cardiac function by calcium handling impairments in models of genetic and dietetic obesity. Methods: The search for articles in electronic databases was performed with key words. Results: Initially studies that showed in title one of the key words were selected for analysis. 23 articles were obtained for reading in full. Then, 18 relevant articles were identified on cardiac dysfunction in obesity, both genetic and dietary and participation of the intracellular calcium handling. Conclusion: The literature presents that both genetic and dietetic obesity promotes cardiac dysfunction modulated by various changes in traffic intracellular Ca2+ and its regulators protein.
Subject(s)
Cardiovascular Diseases/etiology , Calcium/metabolism , Obesity/complications , Calcium/physiology , Leptin/adverse effects , Leptin/physiology , Calcium Channels, L-Type , Heart Disease Risk Factors , Obesity/geneticsABSTRACT
The major cat allergen, Fel d 1, is a structurally complex protein with two N-glycosylation sites that may be filled by different glycoforms. In addition, the protein contains three putative Ca2+ binding sites. Since the impact of these Fel d 1 structure modifications on the protein dynamics, physiology and pathology are not well established, the present work employed computational biology techniques to tackle these issues. While conformational effects brought upon by glycosylation were identified, potentially involved in cavity volume regulation, our results indicate that only the central Ca2+ ion remains coordinated to Fel d 1 in biological solutions, impairing its proposed role in modulating phospholipase A2 activity. As these results increase our understanding of Fel d 1 structural biology, they may offer new support for understanding its physiological role and impact into cat-promoted allergy.