HIDROLASAS ACIDAS PDF

La denominación fosfatasa ácida (EC ) comprende un conjunto de enzimas por su enorme in especificidad, ya que miden la actividad enzimática de las fosfatasas ácidas de los diferentes tejidos y no sólo de la fracción prostática. La manosafosfato (M6P) es un monosacárido derivado de la manosa que se caracteriza por La M6P actúa como señal para las proteínas precursoras de las hidrolasas ácidas que están destinadas para ser transportadas hasta los. Start studying HIDROLASAS. Learn vocabulary, terms, and HIDROLASAS ACIDAS EN DIGESTION MACROMOLECULAS. HIDROLASAS. GLICOSIDASAS.

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Relation of CA polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase FAAH with obesity and insulin resistance. A de Luis, M. The aim of our study was to investigate the relationship of missense polymorphism cDNA C- A of FAAH gene on obesity anthropometric parameters, cardiovascular risk factors and adipocytokines.

An indirect calorimetry, tetrapolar electrical bioimpedance, blood pressure, a serial assessment of nutritional intake with 3 days written food records and biochemical analysis lipid profile, adipocytokines, insulin, CRP and lipoprotein-a were performed.

The statistical analysis was performed for the combined CA and AA as a group and wild type CC as second group. One hundred and ninety four patients No differences were detected between groups in anthropometric parameters and dietary intakes. According to recent surveys, approximately two thirds of the population of Spain is overweight 1.

The current view of adipose tissue is that of an active secretory organ, sending out and responding to signals that modulate appetite, insulin sensitivity, energy expenditure, inflammation and immunity 2. Herbal Cannabis sativa marijuana has been known to have many psychoactive effects in humans including robust increases in appetite and body weight 3. Nevertheless, the mechanism underlying cannabinoid neurobiological effects have been recently revealed 4. The endogenous cannabinoid system mediates and it is positioned both functionally and anatomically 5 to be an important modulator of normal human brain behavior.

The main inactivating enzyme of endogenous cannabinoid receptor ligands is fatty acid amide hydrolase FAAHwhich has been identified as the catabolic enzyme capable of inactivating most of the endocannabinoids 6. The pharmacological effects of some endocannabinoids appear to be regulated by FAAH activity 7suggesting that FAAH has the role to be a modulating enzyme for human behavior.

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However, in a large study sample subjectsJensen et al 11 were unable to find hidrooasas of this polymorphism with overweight or obesity. Considering the evidence that endogenous cannabinoid system plays a role in metabolic aspects of body weight and feeding behavior 12we decided to investigate the association of this FAAH missense polymorphism with obesity and adipocytokines.

These patients were recruited in a Nutrition Clinic Unit and signed an informed consent. Local ethical committee approved the protocol. All patients with a 2 weeks weight-stabilization period before recruitment were enrolled.

Weight, blood pressure, basal glucose, c-reactive protein CRPinsulin, insulin resistance HOMAtotal cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides blood and adipocytokines leptin, adiponectin, resistin, TNF alpha, and interleukin 6 levels were measured at basal time.

A tetrapolar bioimpedance, an indirect calorimetry and a prospective serial assessment of nutritional intake with 3 days written food records were realized. Genotype of FAAH gene polymorphism was studied. Oligonucleotide primers and probes were designed with the Beacon Designer 4. DNA was denaturated at 95 o C for 3 min; this was followed by 50 cycles of denaturation at 95 o C for 15 s, and annealing at The PCR were run in a 25 uL final volume containing Hardy Weinberg equilibrium was assessed.

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Plasma glucose levels were determined by using an automated glucose oxidase method Glucose analyser 2, Beckman Instruments, Fullerton, California. Lipoprotein a was determined by immunonephelometry with the aid adidas a Beckman array analyzer Beckman Instruments, Calif.

Hisrolasas total cholesterol and triglyceride concentrations were determined by enzymatic colorimetric assay Technicon Instruments, Ltd. LDL cholesterol was calculated using Friedewald formula. Normal values of IL6 was 1. For the measurement of resting energy expenditure, subjects were admitted to a metabolic ward. Body weight was measured to an accuracy of 0. Waist narrowest diameter between xiphoid process and iliac crest and hip widest diameter over greater trochanters circumferences to derive waist-to hip ratio WHR were measured, too.

Tetrapolar body electrical bioimpedance was used to determine body composition with an accuracy of 5 g An electric current of 0.

Resistance and reactance gidrolasas used to calculate total body water, fat and fat-free mass. Blood pressure was measured twice after a 10 minutes rest with a random zero mercury sphygmomanometer, and averaged. Patients received prospective serial assessment of nutritional intake with 3 days written food records.

All enrolled subjects received instruction to record their daily dietary intake hidrolasxs three days including a hidrolzsas day. Handling of the dietary data was by means of a personal computer equipped with personal software, incorporating use of food scales and models to enhance portion size accuracy. Records were reviewed by a registered dietitian and analyzed with a computer-based data evaluation system. National composition food tables were used as reference The distribution of variables was analyzed with Kolmogorov-Smirnov test.

Non-parametric variables were analyzed with the U-Mann-Whitney test. A p-value under 0.

Two hundred and seventy nine patients acdias informed consent and were enrolled in the study. The mean age was All subjects were weight stable during the 2 weeks period preceding the study body weight change, 0. Age was similar in both groups wild type: Table I shows the anthropometric variables.

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No differences were detected between groups. Table II shows the classic cardiovascular risk factors. Triglycerides, glucose and HOMA values were higher in wild type group than mutant type group.

Table III shows nutritional intake with 3 days written food records. No statistical differences were detected hidrolaxas caloric, carbohydrate, fat, and protein intakes. Aerobic exercise per week was similar in both groups. Table IV shows levels of adipocytokines. IL-6 levels were higher in wild type group than mutant type group. No differences were detected between both groups in other serum adipocytokine levels.

Since genetic influences are thought to play a greater role in obesity, identification of obesity genes may be more easily detected in the former. Studies of the CA variant and obesity from various authors hidolasas yeldied conflicting results In our study, the percentage of AA genotype 3.

Manosa-6-fosfato

The percentage of AC genotype In our design, we investigated the effect of FAAH genetic variation on weight, and also on metabolic parameters. An association between this polymorphism and metabolic profile has been described. Interestingly, Aberle et al 24 have shown that carriers of the A allele had a significantly greater decrease in the total cholesterol and triglycerides as compared to wild type when folloging a low fat diet.

The lack of association between this polymorphism and anthropometric parameters has been described by other authors. The results of our study agree with those of Jensen et al 11 or Papazoglou et al 25 and contrast with those of Sipe et al 9. It is noteworthy that when BMI was evaluated as a continous variable in subjects, the median BMI was significantly higher in subjects with the AA genotype compared to the median BMI of the other subjects 9.

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The effects of the FAAH AA could result in the upregulation of natural reward behaviours such as consumption of sweets and palatable food associated with overweigth and obesity. Under normal circumstances, brain endocanabinoid signalling may exert tonic control on the levels of certain neurotransmitters. However, the inconsistencies between association studies may reflect the complex interactions between multiple population-specific genetic and environmental factors.

Perhaps, these different results could be explained by inclusion criteria of subjects in previous studies of the literature. These previous studies would require composition analysis of the diet to determine whether dietary components could be responsible for the lipid profile modifications.

In our study dietary intake did not show statistical differences between groups, in this way our datas have been controlled by dietary intake and previous discrepancies could be explain by this uncontrolled factor dietary intake. Accumulating evidence indicates that the endogenous cannabinoid system is an essential homeostatic regulator of energy balance and weight via central appetite-stimulating mechanisms as well as peripheral lipogenesis The anatomical convergence of CB1 receptors and FAAH enzyme activity capable of regulating endocannabinoid tone supports the notion that FAAH is positioned for regulation of endocannabinoid levels that could influence craving and reward behaviors through the relevant neuronal circuitry.

Patients with this polymorphism have half the FAAH enzymatic activity and protein expression when compared with wild-type subjects This provide a link between the consequences of this polymorphism and the present epidemiological study indicating that the FAAH AA polymorphism may play a role in decrease or increase metabolic risk associated to obesity. In our study, the elevation of inflammation markers IL-6 in patients with wild type genotype could be related with an altered postprandial response of fatty acids absorption no measured in our design.

Elevated free hidrolsas acids increases the acummulation acjdas triglycerides in the adipocyte, related with imbalance of lipoprotein lipase activity and overproduction of adipokines such as IL The lack of association of this proimflammatory state with fat mass or BMI could indicate the existence of complex unmeasured gene-gene or gene-environment interactions that may enhance metabolic abnormalities in obese patients.

In conclusion, the novel finding of this study is the association of the mutant type group AC and AA of FAAH with a better cardiovascular profile triglyceride, glucose, interleukine 6 and HOMA levels than wild type group. Further studies are needed to elucidate this complex relationship in an independent way of body mass index. Med clin Barc ; Current Atherosclerosis Reports ; 7: The effects of cannabinnoids on the brain. Cloning and molecular characterization of the rat CB2 cannabinoid receptor.

Biochim Biophys Acta ; Endocannabinoids in the central nervous system an overview.

Fosfatasa ácida – Wikipedia, la enciclopedia libre

Prostaglandins Leukot Essent Fatty acids ; The fatty acid amide hydrolase FAAH 1. Prostaglandins Leukot Essent Fatty Acids ; Pharmacological activity of fatty acid amides is regulated, but not mediated, by fattu acid amide hydrolase in vivo. Pharmacol Exp Ther ; A Missense mutation hidrolasws human fatty acid amide hydroxylase associated with caidas drug abuse.

Overweight and obesity associated with a missense polymorphism ain fatty acd amide hydrolase FAAH. Inte J of Obes ;

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