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Carbohydrate Metabolism

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Cấu trúc

  • Carbohydrate Metabolism

  • Glycolysis

    • Anaerobic Respiration

    • Aerobic Respiration

  • Krebs Cycle/Citric Acid Cycle/Tricarboxylic Acid Cycle

  • Oxidative Phosphorylation and the Electron Transport Chain

  • Gluconeogenesis

  • Chapter Review

  • Review Questions

  • Critical Thinking Questions

Nội dung

NĂNG L NG SINH H CƯỢ Ọ Lipid Metabolism (TRAO Đ I LIPID) ỔI. Đ i c ng v lipidạ ươ ề :1. Đ nh nghĩaị :Lipid là nh ng h p ch t c a axit béo v i ancol ho c ữ ợ ấ ủ ớ ặaminoacol.2. Hàm l ng:ượTrong c th s ng Lipid d tr mô m chi m t 70 – 90 ơ ể ố ự ữ ở ỡ ế ừ%. Trong t y s ng, não hàm l ng Lipid cũng khá cao chi m ủ ố ượ ết 14 – 20% kh i l ng t i, ngoài ra còn có trong tr ng, ừ ố ượ ươ ứtinh trùng,… Trong các h t có d u, hàm l ng Lipid r t cao ạ ầ ượ ấnh h t th u d u có kho ng 65 – 70%, v ng 48 – 63%, l c ư ạ ầ ầ ả ừ ạ40 – 60%, đ u t ng 18%. Hàm l ng d u trong th c v t ậ ươ ượ ầ ự ậthay đ i nhi u theo gi ng, cách chăm bón và th i gian thu ổ ề ố ờho ch.ạ 3. Ch c năngứ :- Làm nguyên li u cung c p năng l ng cho c ệ ấ ượ ơth s ng có giá tr ca nh t (9,3 kcal/g) so v i ể ố ị ấ ớgluxit (4,1 kcal/g) và protein (4,2 kcal/g). - Đ ng th i v i l p m d i da có tác d ng cách ồ ờ ớ ớ ỡ ướ ụnhi t đ gi nhi t cho c th .ệ ể ữ ệ ơ ể- Là thành ph n c u t o quan tr ng c a các ầ ấ ạ ọ ủmàng t bàoế- Gi vai trò sinh h c c c kì quan tr ng: làm ch t ữ ọ ự ọ ấtr giúp (cofactor) ho t đ g xúc tác c a enzyme, ợ ạ ộ ủch t v n chuy n đi n t , là s c t h p thu ánh ấ ậ ể ệ ử ắ ố ấsáng, y u t nh hóa, hormon và các ch t v n ế ố ữ ấ ậchuy n thông tin n i bàoể ộ Lipogenesis and LipolysisLipogenesis and LipolysisFigure 24.14 Lipid thu nầ :+ glixerin: este c a glixerin và axit béo.ủ+ Xerit (sáp):este c a axit báo v i ancol có kh i l ng phân ủ ớ ố ượt l n.ử ớ+ Sterit : este c a axit béo v i ancol m ch vòng (cholesterol)ủ ớ ạLipid t pạ :+ Phospholipid: có ch a thêm m t g c axit phosphoric, thông ứ ộ ốth ng kèm theo các bazo nit và các nhóm th khác.ườ ơ ếGlixerolphotpholipit: ancol là glixerinSphingophotpholipit: ancol là Sphigozin+ Glicolipit: có ch a m t axis béo, sphingozin, và đ ng.ứ ộ ườ+ Các Lipid ph c t p khác: Sulfolipit, aminolipit, lipoprotein . ứ ạ 4. Phân lo i: ạ g m 2 ồlo iạ M T S AXIT BÉO SINH H C QUAN TR NGỘ Ố Ọ Ọ II. TRAO Đ I LIPID: Ổ (Lipid Metabolism)1. Năng l ng phân gi i Lipid:ượ ảPhân gi i ch t béo bao g m 2 ph n: là phân gi i ả ấ ồ ầ ảph n glixerin hay sphingozin và ph n axit béo. ầ ầT ng ph n riêng cũng có nh ng v n đ r t ph c t p ừ ầ ữ ấ ề ấ ứ ạnh phân gi i axit béo no, axit béo không no, axit béo ư ảcó s cacbon ch n, axit béo có s cácbon l , axit béo ố ẵ ố ẻđ n gi n, axit béo ph c t p…. gi a chúng ít nhi u ơ ả ứ ạ ữ ềkhác nhau trong cách phân gi iả Ví d : Năng l ng c a quá trình ụ ượ ủ  -oxy hóa axit béo V nguyên t c cũng t ng t nh oxy hóa glucose là ề ắ ươ ự ưc n năng l ng đ ho t hóa ban đ u. Nh ng quá trình này ầ ượ ể ạ ầ ưkhác oxy hóa glucose nh sau:ư- Khi ho t hóa m t phân t ạ ộ ửaxit béo tiêu hao năng l ng ượtrong m i liên k t ố ế  –phosphat c a ATP ủ- Giai đo n đ u ho t hóa, năng ạ ầ ạl ng chuy n t ATP đ n axit ượ ể ừ ếbéo không đ phosphoril hóa ểnh glucose thành glucose – 6 ư ởphosphat mà đ t o thành s n ể ạ ảph m axit béo – axyl – CoA ẩCOO−1234αβγ fatty acid with a cis-∆9 double bond [...]... b năng ạ ầ ầ ậ ộ l ng đ c gi i phóng ra khi phân gi i ượ ượ ả ả  c a axit béo là ủ Năng l ng (tính b ng ATP): 5(n/1-1) + 12n/2 -1ượ ằ Ví d : Năng l ng c a q trình ụ ượ ủ  -oxy hóa axit béo V nguyên t c cũng t ng t nh oxy hóa glucose là ề ắ ươ ự ư c n năng l ng đ ho t hóa ban đ u. Nh ng quá trình này ầ ượ ể ạ ầ ư khác oxy hóa glucose nh sau:ư - Khi ho t hóa m t phân t ạ ộ ử axit béo tiêu hao năng. .. axit panmitic (C16) và stearic ủ (C18). Đ c đi m c a h enzyme xúc tác quá trình này là ặ ể ủ ệ c n có oxy phân t và m t coenzyme kh (NADPH +H+) ầ ử ộ ử tham gia T ng quátổ Lipid Metabolism (TRAO Đ I LIPID) Ổ I. Đ i c ng v lipidạ ươ ề : 1. Đ nh nghĩaị : Lipid là nh ng h p ch t c a axit béo v i ancol ho c ữ ợ ấ ủ ớ ặ aminoacol. 2. Hàm l ng:ượ Trong c th s ng Lipid d tr mô m chi m t 70 – 90... Carbohydrate Metabolism Carbohydrate Metabolism Bởi: OpenStaxCollege Carbohydrates are organic molecules composed of carbon, hydrogen, and oxygen atoms The family of carbohydrates includes both simple and complex sugars Glucose and fructose are examples of simple sugars, and starch, glycogen, and cellulose are all examples of complex sugars The complex sugars are also called polysaccharides and are made of multiple monosaccharide molecules Polysaccharides serve as energy storage (e.g., starch and glycogen) and as structural components (e.g., chitin in insects and cellulose in plants) During digestion, carbohydrates are broken down into simple, soluble sugars that can be transported across the intestinal wall into the circulatory system to be transported throughout the body Carbohydrate digestion begins in the mouth with the action of salivary amylase on starches and ends with monosaccharides being absorbed across the epithelium of the small intestine Once the absorbed monosaccharides are transported to the tissues, the process of cellular respiration begins ([link]) This section will focus first on glycolysis, a process where the monosaccharide glucose is oxidized, releasing the energy stored in its bonds to produce ATP 1/18 Carbohydrate Metabolism Cellular Respiration Cellular respiration oxidizes glucose molecules through glycolysis, the Krebs cycle, and oxidative phosphorylation to produce ATP Glycolysis Glucose is the body’s most readily available source of energy After digestive processes break polysaccharides down into monosaccharides, including glucose, the monosaccharides are transported across the wall of the small intestine and into the circulatory system, which transports them to the liver In the liver, hepatocytes either pass the glucose on through the circulatory system or store excess glucose as glycogen Cells in the body take up the circulating glucose in response to insulin and, through a series of reactions called glycolysis, transfer some of the energy in glucose to ADP to form ATP ([link]) The last step in glycolysis produces the product pyruvate 2/18 Carbohydrate Metabolism Glycolysis begins with the phosphorylation of glucose by hexokinase to form glucose-6-phosphate This step uses one ATP, which is the donor of the phosphate group Under the action of phosphofructokinase, glucose-6-phosphate is converted into fructose-6-phosphate At this point, a second ATP donates its phosphate group, forming fructose-1,6-bisphosphate This six-carbon sugar is split to form two phosphorylated three-carbon molecules, glyceraldehyde-3-phosphate and dihydroxyacetone phosphate, which are both converted into glyceraldehyde-3-phosphate The glyceraldehyde-3-phosphate is further phosphorylated with groups donated by dihydrogen phosphate present in the cell to form the three-carbon molecule 1,3-bisphosphoglycerate The energy of this reaction comes from the oxidation of (removal of electrons from) glyceraldehyde-3-phosphate In a series of reactions leading to pyruvate, the two phosphate groups are then transferred to two ADPs to form two ATPs Thus, glycolysis uses two ATPs but generates four ATPs, yielding a net gain of two ATPs and two molecules of pyruvate In the presence of oxygen, pyruvate continues on to the Krebs cycle (also called the citric acid cycle or tricarboxylic acid cycle (TCA), where additional energy is extracted and passed on 3/18 Carbohydrate Metabolism Glycolysis Overview During the energy-consuming phase of glycolysis, two ATPs are consumed, transferring two phosphates to the glucose molecule The glucose molecule then splits into two three-carbon compounds, each containing a phosphate During the second phase, an additional phosphate is added to each of the three-carbon compounds The energy for this endergonic reaction is provided by the removal (oxidation) of two electrons from each three-carbon compound During the energy-releasing phase, the phosphates are removed from both three-carbon compounds and used to produce four ATP molecules 4/18 Carbohydrate Metabolism Watch this video to learn about glycolysis Glycolysis can be divided into two phases: energy consuming (also called chemical priming) and energy yielding The first phase is the energy-consuming phase, so it requires two ATP molecules to start the reaction for each molecule of glucose However, the end of the reaction produces four ATPs, resulting in a net gain of two ATP energy molecules Glycolysis can be expressed as the following equation: Glucose + 2ATP + 2NAD+ + 4ADP + 2Pi → Pyruvate + 4ATP + 2NADH + 2H+ This equation states that glucose, in combination with ATP (the energy source), NAD+ (a coenzyme that serves as an electron acceptor), and inorganic phosphate, breaks down into two pyruvate molecules, generating four ATP molecules—for a net yield of two ATP—and two energy-containing NADH coenzymes The NADH that is produced in this process will be used later to produce ATP in the mitochondria Importantly, by the end of this ...Int. J. Med. Sci. 2011, 8 http://www.medsci.org 295 IInntteerrnnaattiioonnaall JJoouurrnnaall ooff MMeeddiiccaall SScciieenncceess 2011; 8(4):295-301 Research Paper Effects of p-Synephrine alone and in Combination with Selected Bioflavo-noids on Resting Metabolism, Blood Pressure, Heart Rate and Self-Reported Mood Changes Sidney J. Stohs1, Harry G Preuss2, Samuel C. Keith3, Patti L. Keith3, Howard Miller4, Gilbert R. Kaats3 1. Dean Emeritus, Creighton University Health Sciences Center, Omaha, NE 68178, USA 2. Department of Physiology, Georgetown University Medical Center, Washington, DC, USA 3. Integrative Health Technologies, Inc., 4940 Broadway, San Antonio, TX 78209, USA 4. Nutratech Inc., West Caldwell, NJ 07006, USA  Corresponding author: Harry G. Preuss, M.D., preusshg@georgetown.edu, phone: 1-202-687-1441 © Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/ licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited. Received: 2011.02.02; Accepted: 2011.03.06; Published: 2011.04.28 Abstract Bitter orange (Citrus aurantium) extract is widely used in dietary supplements for weight management and sports performance. Its primary protoalkaloid is p-synephrine. Most studies involving bitter orange extract and p-synephrine have used products with multiple ingredients. The current study assessed the thermogenic effects of p-synephrine alone and in conjunction with the flavonoids naringin and hesperidin in a double-blinded, randomized, place-bo-controlled protocol with 10 subjects per treatment group. Resting metabolic rates (RMR), blood pressure, heart rates and a self-reported rating scale were determined at baseline and 75 min after oral ingestion of the test products in V-8 juice. A decrease of 30 kcal occurred in the placebo control relative to baseline. The group receiving p-synephrine (50 mg) alone exhibited a 65 kcal increase in RMR as compared to the placebo group. The consumption of 600 mg naringin with 50 mg p-synephrine resulted in a 129 kcal increase in RMR relative to the placebo group. In the group receiving 100 mg hesperidin in addition to the 50 mg p-synephrine plus 600 mg naringin, the RMR increased by 183 kcal, an increase that was statistically sig-nificant with respect to the placebo control (p<0.02). However, consuming 1000 mg hes-peridin with 50 mg p-synephrine plus 600 mg naringin resulted in a RMR that was only 79 kcal greater than the placebo group. None of the treatment groups exhibited changes in heart rate or blood pressure relative to the control group, nor there were no differences in self-reported ratings of 10 symptoms between the treatment groups and the control group. This unusual finding of a thermogenic combination of ingredients that elevated metabolic rates without corresponding elevations in blood pressure and heart-rates warrants longer term studies to assess its value as a weight control agent. Key words: p-Synephrine, naringin, hesperidin, resting metabolic rate, heart rate, blood pressure Introduction The bioflavonoids hesperetin and naringenin are widely distributed in citrus fruits and juices as their glycosides, hesperidin and naringin, Elucidation of the role of fructose 2,6-bisphosphate in the regulation of glucose fluxes in mice using in vivo 13 C NMR measurements of hepatic carbohydrate metabolism In-Young Choi 1 , Chaodong Wu 2 , David A. Okar 2 , Alex J. Lange 2 and Rolf Gruetter 1,3 6 Departments of Radiology 1 , Biochemistry, Molecular Biology and Biophysics 2 , Neuroscience 3 , University of Minnesota Medical School, Minneapolis, MN, USA Fructose 2,6-bisphosphate (Fru-2,6-P 2 ) plays an important role in the regulation of major carbohydrate fluxes as both allosteric activator and inhibitor of target enzymes. To examine the role of Fru-2,6-P 2 in the regulation of hepatic carbohydrate metabolism in vivo,Fru-2,6-P 2 levels were elevated in ADM mice with adenovirus-mediated overex- pression of a double mutant bifunctional enzyme, 6-phos- phofructo-2-kinase/fructose-2,6-bisphosphatase (n ¼ 6), in comparison to normal control mice (control, n ¼ 6). The rates of hepatic glycogen synthesis in the ADM and control mouse liver in vivo were measured using new advances in 13 C NMR including 3D localization in conjunction with [1- 13 C]glucose infusion. In addition to glycogen C1, the C6 and C2–C5 signals were measured simultaneously for the first time in vivo, which provide the basis for the estimation of direct and indirect synthesis of glycogen in the liver. The rate of label incorporation into glycogen C1 was not different between the control and ADM group, whereas the rate of label incorporation into glycogen C6 signals was in the ADM group 5.6 ± 0.5 lmolÆg )1 Æh )1 , which was higher than that of the control group of 3.7 ± 0.5 lmolÆg )1 Æh )1 (P < 0.02). The rates of net glycogen synthesis, determined by the glycogen C2–C5 signal changes, were twofold higher in the ADM group (P ¼ 0.04). The results provide direct in vivo evidence that the effects of elevated Fru-2,6-P 2 levels in the liver include increased glycogen storage through indirect synthesis of glycogen. These observations provide a key to understanding the mechanisms by which elevated hepatic Fru-2,6-P 2 levels promote reduced hepatic glucose production and lower blood glucose in diabetes mellitus. Keywords: 1 NMR; in vivo; fructose-2, 6-bisphosphate; gly- cogen; mouse liver. The regulation of carbohydrate metabolism in the liver is important for blood glucose homeostasis by controlling hepatic glucose production. This involves an intricate regulation of metabolic pathways, such as glycolysis, gluconeogenesis, glycogenesis and glycogenolysis in the liver [1,2]. The balance of these pathways is severely altered in patients with type II diabetes mellitus contributing to chronically elevated plasma glucose concentrations. There- fore, an understanding of the regulation of these fluxes can provide important insights into the mechanisms and poten- tial treatment of diabetes. The rates of glycolysis and gluconeogenesis are important in the rate of hepatic glucose production. Fructose-2,6- bisphosphate (Fru-2,6-P 2 ) plays an important role through its reciprocal allosteric effects on two critical enzymes, 6-phosphofructo-1-kinase and fructose-1,6-bisphosphatase (reviewedin[3]).Fru-2,6-P 2 activates phosphofructo-1- kinase to stimulate glycolysis and inhibits fructose-1,6- bisphosphatase to reduce gluconeogenesis. Synthesis as well as RESEARC H Open Access A systems biology approach to analyse leaf carbohydrate metabolism in Arabidopsis thaliana Sebastian Henkel 1† , Thomas Nägele 2*† , Imke Hörmiller 2 , Thomas Sauter 3 , Oliver Sawodny 1 , Michael Ederer 1 and Arnd G Heyer 2 Abstract Plant carbohydrate metabolism comprises numerous metabolite interconversions, some of which form cycles of metabolite degradation and re-synthesis and are thus referred to as futile cycles. In this study, we present a systems biology approach to analyse any possible regulatory principle that operates such futile c ycles based on experimental data for sucrose (Scr) cycling in photosynthetically active leaves of the model plant Arabidopsis thaliana. Kinetic parameters of enzymatic steps in Scr cycling were identified by fitting model simulations to experimental data. A statistical analysis of the kinetic parameters and calculated flux rates allowe d for estimation of the variability and supported the predictability of the model. A principal component analysis of the parameter results revealed the identifiability of the model parameters. We investigated the stability properties of Scr cycling and found that feedback inhibition of enzymes catalysing metabolite interconversions at different steps of the cycle have differential influence on stability. Applying this observation to futile cycling of Scr in leaf cells points to the enzyme hexokinase as an important regulator, while the step of Scr degradation by invertases appears subordinate. Keywords: Systems biology, carbohydrate metabolism, Arabidopsis thaliana, kinetic modelling, stability analysis, sucrose cycling Introduction Plant metabolic pathways are highly complex, compris- ing various branch points and c rosslinks, and thus kinetic modelling turns up as an adequate tool to inves- tigate regulatory principles. Recently, we presented a kinetic modelling approach to investi gate core reacti ons of primary carbohydrate metabolism in photosyntheti- cally active leaves of the model plant Arabidopsis thali- ana [1] with an emphasis on the physiological role of vacuolar invertase, an enzyme that is involved in degra- dation of sucrose (Scr). This model was developed in an iterative process of modelling a nd validation. A final parameter s et was identified allowing for simulation of the main carbohydrate fluxes and interpretation of the system behaviour over diurnal cycles. We found that Scr degradation by vacuolar invertase and re-synthesis involving phosphorylation of hexoses (Hex) allows the cell to balance deflections of metabolic homeostasis dur- ing light-dark cycles. In this study, we investigate the structural and stability properties of a model derived from the Scr cycling part of the metabolic pathway described in [1]. Based on the existing model structure, model parameters were repeat- edly adjusted in an automated process applying a para- meter identification algorithm to match the measured and s imulated data. A method for statistical evaluation of the parameters and simulation results is introduced, which allows for the estimation of parameter variability. Statistical evaluation demonstrates that the same nom- inal concentration courses are predicted for dif ferent identification runs, while small variability in fluxes and larger variability in parameters can be observed. Further, the parameter i dentification results were analysed apply- ing a principal component analysis (PCA). This leads to a more extensive investigation with respect to the exten- sion and alignment of the parameter values Carbon partitioning: fructose 2,6-bisphosphate content as an indicator of specific changes in carbohydrate metabolism in needles from class II spruce trees W. Einig R. Hampp Universitit Tubingen, Biochemie der Pflanzen, Auf der Morgenstelle 1, D-7400 Tobingen, F.R.G. Introduction It has been shown that very low doses of airborne pollutants (ozone, sulfite) can significantly change source-sink relation- ships. These shifts in allocation or trans- portation out of leaves can occur prior to reductions in photosynthesis (ozone; Mcl_aughlin and McConathy, 1983) and can take place within minutes (Minchin and Gould, 1986). In spite of intense research in this area, there is, however, only little information available about metabolic acclimation of tissues to pollutants. It has thus been our aim to screen for biochemical indications of altered patterns of carbon allocation in needles of Norway spruce (Picea abies). Materials and Methods The materials used for our investigations were needles from spruce trees from 2 locations in the southern part of the Black Forest (Kalbele- scheuer and Haldenhof, near Freiburg, F.R.G.). Collection and freeze-drying of needle samples as well as metatrolite analyses were as descri- bed elsewhere (Einig and Hampp, 1988; Hampp etaL, 1989). Results and Discussion Season- and age-dependent variations in pool sizes There is considerable evidence that the rate of starch synthesis is controlled by the rates of sucrose formation and trans- port. Metabolites involved in the regulation of carbon partitioning between starch and sucrose are triose phosphates (TP; dihy- droxyacetone phosphate, glyceraldehyde 3-phosphate), glyceric acid 3-phosphate (PGA), fructose 6-phosphate (F6P), ortho- phosphate (P i) and pyrophosphate (PP i ). Levels of these metabolites control syn- thesis and degradation of the most impor- tant regulator, fructose 2,6-bisphosphate (F26BP). This compound affects cytosolic sucrose synthesis by inhibiting the fruc- tose bisphosphatase (FBPase) reaction (gluconeogenesis) and activating a PP i- dependent phosphofructokinase (PFP; ac- tive in both directions, glycolysis and glu- coneogenesis (for a review see Stitt, 1987; compare also Fig. 1 ). Sucrose and starch as ’endpoints’ of this regulatory system show distinct dif- ferences in their pool sizes. Needles from control trees have optimum starch levels in early summer (Fig. 2a). Independent of needle age, there is a continuous decline towards October. Sucrose, in contrast, is much more constant in its seasonal pool sizes (Fig. 2b). There are, however, specific differences, when pool sizes of phosphorylated inter- mediates are compared. An intimate cor- relation between pool sizes of TP, F6P and F26BP is observed when the average contents of all needles (1980-1985) are plotted versus the sampling date (Fig. 3). Under the assumption that the changes in pool sizes observed for F6P and TP also occur in the cytosol of our needle mesophyll cells, all these observations can easily be explained by the scheme shown in Fig. 1. In June samples, e.g., starch, F6P and F26BP are high, while TP are low; high levels of F6P, possibly indi- cative of limited sucrose export (rates of synthesis exceed rates of export), activate F26BP synthesis. Increased levels of F26BP, however, favor glycolysis over glu- coneogenesis and thus TP are diverted into starch synthesis. In July, in contrast, an opposite situation emerges with decreased amounts of F6P and F26BP and high levels of TP. This metabolic situation should thus be indicative of ... aerobic respiration, a net total of 36 ATPs are produced ([link]) 12/18 Carbohydrate Metabolism Carbohydrate Metabolism Carbohydrate metabolism involves glycolysis, the Krebs cycle, and the electron... pathway or be used by the liver as a substrate for gluconeogenesis 14/18 Carbohydrate Metabolism Gluconeogenesis 15/18 Carbohydrate Metabolism Gluconeogenesis is the synthesis of glucose from pyruvate,... under conditions of fasting, starvation, and low carbohydrate diets So, the question can be raised as to why the body would 13/18 Carbohydrate Metabolism create something it has just spent a fair

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