Ograniczanie wyników

Czasopisma help
Autorzy help
Lata help
Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 51

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 3 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych:  metabolic disease
help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 3 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
Mitochondrial homeostasis, resulting from fusion and fission processes together with mitophagy and mitogenesis, are widely studied nowadays. This is probably because we know more and more about the role of mitochondria in metabolic diseases (diabetes, hypertension), neurodegeneration (Parkinson’s Disease, Alzheimer’s Disease), but also in broad spectrum of inherited neurological syndromes (CharcotMarie-Tooth). In our studies we aimed to examine the expression pattern of particular mitochondrial proteins, mitofusin 1 (Mfn1) and mitofusin 2 (Mfn2), in mouse tissues. We aim to verify, whether potential differences in expression of those proteins can by implicated in pathomechanism of Charcot-Marie-Tooth type 2A neuromyopathy, related to mitofusion 2 gene mutations. Mitofusins are mitochondrial GTPases, implicated in fusion of outer mitochondrial membrane. In this process, mitofusins juxtapose two mitochondria by combining homo- and heterodimers at the surface of two outer mitochondrial membranes. Although there is 63% homology between mitofusins, it is proved, that they show some different functions. As Mfn1 KO present more severe aberrations in mitochondrial network formation than Mfn2 deficient cells, Mfn1 is considered to have stronger fusion activity. It is also suspected, that it is Mfn1 that links fusion of outer and inner mitochondrial membranes. Nevertheless, Mfn2, but not Mfn1, is present at endoplasmic reticulum (ER). Mfn2 tethers ER to mitochondria facilitating calcium flux and (indirectly) autophagy. Moreover, Mfn2 seems to have some regulatory effect on cell cycle, beyond its fusion activity and its lower expression seems to correlate with insulin resistance and hyper proliferation in hypertension. So, the question is, how much these two proteins can replace each other while playing so different roles? Moreover, it is suggested that CMT2A predominantly affects peripheral nerves because mutated, malfunctioned Mfn2 is insufficiently compensated by Mfn1 due to its low expression particularly in this type of tissue. To discuss this issue, we have investigated the expression of Mfn1 and Mfn2, as well as protein content, in tissues, performing Real Time PCR and Western Blot studies. Preliminary data from Western blot analysis displayed equally high relative level of both mitofusins in nervous system (dorsal root ganglia, cerebral cortex, cerebellum, spinal cord) in comparison to peripheral organs (muscle, heart, liver, kidney, skin). Moreover, Mfn1 expression seems significantly lower in dorsal root ganglia, which are well established model of peripheral nervous system. This phenomenon was not observed for other tissues, even from central nervous system. So it seems quite possible, that axonal damage of peripheral nerves in CMT2A, may be observed due to the poor compensation of dysfunctional Mfn2 by fully functional Mfn1, which is not expressed at sufficient level. The project was supported by NSC grant NN402474640
The frequency of obesity occurrence is constantly increasing all over the world and becoming global epidemic. Facing the lack of the efficiency of conservative treatment, patients with II and III degree of obesity are qualified for surgical treatment; however, the efficiency of surgical treatment is connected with permanent change of nutritional habits and previous lifestyle of the patient. Modification of the way of nutrition, regardless of the type of bariatric procedure, should especially include the lowering of food energetic value and change of type, consistency and size of consumed food. Nutritional treatment after bariatric procedures is multistage. It includes clear liquid diet, full liquid diet, pureed diet, mechanically altered soft diet and regular diet. Gradual expanding of the diet protects gastrointestinal tract from chemical, mechanical and thermal irritation by the food. It also should prevent nutritional deficiencies. Significant influence on the result of surgical treatment of obesity has also regular intake of food, consuming products with high nutritional value, avoiding confectionery and fat products, consuming proper amounts of protein (60-80 g/day) and vitamin-mineral supplementation.
Introduction. Diabetes as a non-infectious chronic metabolic disease is a problem of the contemporary world, including Poland. Behaviour therapy plays an important role in its treatment, i.e. proper diet and regular physical activity. Patient’s knowledge of nutrition principles is also an essential complement to the treatment, reducing the risk of late complications of diabetes. Objective. Assessment of the nutrition knowledge of patients with type 1 and type 2 diabetes. Materials and method. The study involved 300 randomly selected patients from Rzeszów and the surrounding area (135 patients with type 1 diabetes and 165 patients with type 2 diabetes) aged 8–78.The analysis was made using a survey questionnaire prepared by the authors of the study, conducted in the period July – December 2011. Results. The survey revealed that patients with type 1 diabetes have greater nutrition knowledge and knowledge about diabetes than patients with type 2 diabetes. On the other hand, they are less likely to comply with the recommendations of the diet prescribed by a doctor or a dietician. Conclusions. Patients with diabetes, regardless of age, type of diabetes, gender, or disease duration require continuous broadening of diabetes knowledge. Systematic training will teach patients proper eating habits related to their diet and lifestyle.
Triketone herbicides are inhibitors of 4-hydroxyphenylpyruvate dioxygenase (HPPD), a key enzyme of the tyrosine transformation pathway, common for plants and animals. One of these herbicides, 2-[2-nitro-4-(trifluoromethyl)benzoyl]-1,3-cyclohexanedione (NTBC), is so selective and efficient that it can be applied as a medicine in a hereditary metabolic disease - tyrosinemia type I. In this paper the available information concerning the molecular mechanism of HPPD inhibition by NTBC, originating from experimental investigations as well as theoretical modeling, has been collected. It is supplemented by results of additional theoretical DFT and/or MP2 calculations of the energetic effects of individual elementary molecular transformations. All these data are discussed and a consistent picture of HPPD inhibition by NTBC is proposed.
9
Content available remote

Neuro-hormonal control of food intake; basic mechanisms and clinical implications

72%
Obesity is one of the most common metabolic diseases and the greatest threats of the health because of possibility of numerous complications. In order to design effective drugs or apply the helpful surgical procedure it is essential to understand physiology of appetite control and pathophysiology of obesity. According to the first law of thermodynamics, the energy input in the form of food, equals energy expenditure through exercise, basal metabolism, thermogenesis and fat biosynthesis. The control of body weight actually concerns the control of adipose tissue with the key role of hypothalamus, possessing several neuronal centers such as that in lateral hypothalamic nuclei considered to be "hunger" center and in ventromedial nuclei serving as the "satiety" center. In addition, paraventricular and arcuate hypothalamic nuclei (ARC) are the sites where multiple hormones, released from the gut and adipose tissue, converge to regulate food intake and energy expenditure. There are two distinct types of neurons in ARC that are important in control of food intake; (1) preopiomelanocortin (POMC) neurons activated by anorexigenic hormones and releasing a-melanocyte-stimulating hormone (alpha-MSH) in satiety center and (2) neurons activated by orexigenic peptides such as ghrelin that release the substances including neuropeptide Y (NPY) and Agouti-Related Peptide (AgRP) in hunger center. ARC integrates neural (mostly vagal) and humoral inputs such as enteropeptides including orexigenic (ghrelin and orexins) and anorexigenic peptides (cholecystokinin, polypeptide YY, glucagon-like peptide-1, oxyntomodulin, leptin and others) that exert a physiological role in regulating appetite and satiety. The peripherally (gut, adipose tissue) and centrally expressed modulators of appetitive behavior act through specific receptors in the afferent (mostly vagal) nerves and hypothalamic neurons implicated in adiposity signaling and regulation of food intake.
Background. Some of the main nutritional reasons for recommending a Mediterranean diet is to prevent metabolic diseases arising through free radical formation. A key constituent compound is β-carotene which, amongst the carotenoids, displays the greatest provitamin A activity as well as possessing significant antioxidant properties. Objectives. Principally, to determine the relationship between serum β-carotene levels and the effect of Mediterranean diet guidelines in a selected group of women. Materials and Methods. The subject group consisted of 26 women aged 19-22 years. A nutritional assessment was performed using 3 day repeats of 24-hour recall interviews. A 9-point aMED (alternate Mediterranean Diet) score was used to study dietary habits. Serum β-carotene was measured by liquid chromatography with photodiode array detection (HPLC-PDA). Results. β-carotene dietary intake was highly variable, ranging from 734 to 14476 μg/day (median 3022 μg/day). Serum β-carotene concentration ranged between 0.071-1.905 μmol/L (median 0.519 μmol/L) and was significantly associated with the Mediterranean Diet model (Spearman r=0.633, p<0.001). Out of the dietary sources of β-carotene, consuming carrots had the most significant impact on its serum concentration. Other dietary factors positively affecting serum β-carotene were: consumption of nuts and seeds, pulses, a favourable ratio of mono-unsaturated fatty acids to saturated fatty acids and eating fruit and wholegrain cereal products. Conclusions. Adopting a Mediterranean-based diet had a positive effect on increasing serum beta-carotene levels.
Phenylketonuria is an inherited metabolic disease, which is characterized by increased level of serum phenylalanine (Phe). The quantitative measurement of Phe in the serum is necessary to confirm the disease, and to distinguish phenylketonuria from other forms of hyperphenylalaninemia. In this study, we report a rapid and inexpensive micro-assay for simultaneous detection and quantitative measurement of serum Phe in dry blood-spots. Analysis of the standard curve showed a broad linear Phe range of 120-1800 µmol L⁻¹. Application of this method in conjunction with the standard Guthrie bacterial inhibition assay and high-pressure liquid chromatography in analyzing 34 samples from phenylketonuria patients and control samples produced comparable results, with the regression equation of Y= 0.994X + 0.996. The advantage of this method over the Guthrie bacterial inhibition assay is its ability to measure the serum Phe quantitatively without false positive results. The method was successfully applied to dried blood-spots as well as serum and whole blood samples. The cost per sample is about 20-50 US cents, which is much less than those of high-pressure liquid chromatography and enzymatic commercial kits. The method can be automated, which is suitable for neonatal and mass phenylketonuria screening, especially in developing countries, where funding is a limiting factor.
Hereditary tyrosinemia type I (HT I, McKusick 276700) is a metabolic disease with a pattern of autosomal recessive inheritance. The disease is caused by a deficiency of the enzyme involved in the last step in the degradation of the amino acid tyrosine, fumarylacetoacetate hydrolase (FAH). The result of this block is the accumulation of catabolites some of which have been proposed to be highly toxic due to their alkylating potential. In humans, hereditary tyrosinemia is often associated with the development of hepatocellular carcinoma in young patients. The reasons for the high incidence of hepatocellular carcinoma are unknown but it has been suggested that it may be caused by accumulated metabolites such as fumarylacetoacetate (FAA) and maieylace­toacetate (MAA). The various mutational defects in the FAH gene are reviewed. The use of two mouse models of this disease to study the molecular basis of the pathologies associated with HT I are discussed. Finally, some preliminary data on the mutagenic potential of FAA and MAA in a gene reversal assay are presented.
The utility of biochemical markers of bone metabolism has not been proven in the diagnosis of metabolic diseases of the bone tissue; however they are widely used as a tools for treatment monitoring. Their serum concentrations are influenced by a number of factors, like gender, health status, anthropometric and environmental factors. All the factors listed above should be taken into consideration during clinical use. The aim of the study was to determine the reference values and evaluate the influence of environmental and anthropometric variables on biochemical markers of bone turnover for women from Lublin Region (Poland). Subjects of the study were 188 normal women aged 30-79, all residents of Lublin Region. Analysed markers of bone turnover were: osteocalcin (OC) and C-terminal cross-linking telopeptide of type I collagen (CTX-I), both assessed using ELISA method. All blood samples were taken and analyzed at the Clinical Chem. Laboratory and Patho-morphology Department at the Institute of Agricultural Medicine in Lublin. The lumbar spine (L2-L4) of all subjects was examined in a-p position using the dual X-ray absorptiometry-DXA (DPX-A LUNAR Corp.) at the Department of Metabolic and Degenerative Diseases of Bone Tissue of Institute of Agricultural Medicine in Lublin. Data pertaining to factors affecting bone tissue were collected using a specially prepared questionnaire. Serum levels of OC and CTX-I in women in every age range were different, generally increasing with age. Serum levels of OC and CTX-I in the analysed population strongly depended of both menopausal status and bone mineral density. In conclusion, this study demonstrates that age and menopausal status variations need to be considered when interpreting laboratory measurements of biochemical markers of bone metabolism.
Retinoic acid-induced osteoporosis (RBM) is one of the most common causes of secondary osteoporosis. This study tested the anti-osteoporetic effect of quercetin in RBM-induced bone loss model (RBM). After 14-day supplementation of 13cRA to induce RBM, rats were administered with quercetin (100 mg/kg) or alendronate (40 mg/kg). We analysed changes in body and uterine weight of animals, femoral geometric characteristics, calcium and phosphorus content, bone weight index, bone hystology, bone mineral density (BMD), markers of bone turnover, lipid peroxidation, glutathione levels and SOD, CAT activity of liver, kidney spleen, and ovary as well as biochemical and haematological variables. In comparison to the control RBM rats, the treatment with quercetin increased bone weight index, BMD, osteocalcin level, femoral geometric characteristics, calcium and phosphorus content in the 13cRA-induced bone loss model. Histological results showed its protective action through promotion of bone formation. According to the results, quercetin could be an effective substitution for alendronate in 13cRA-induced osteoporosis. Good therapeutic potential of quercetin on rat skeletal system is based partly on its antioxidant capacity and estrogenic activity.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 3 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.