> Physiology > Molecular Function > Gluconeogenesis

Gluconeogenesis

Q: What is the purpose of Gluconeogenesis?

Gluconeogenesis is a crucial metabolic process that generates glucose from non-carbohydrate precursors, such as amino acids, lactate, and glycerol. This pathway helps maintain blood glucose levels during periods of fasting or starvation, ensuring the body has a steady supply of glucose for essential functions.

Q: How can PubCompare.ai help with Gluconeogenesis research?

PubCompare.ai is an innovative AI-driven platform that can optimize your Gluconeogenesis research in several ways: 1. It allows you to screen protocol literature more efficiently, helping you quickly locate relevant protocols from literature, preprints, and patents. 2. The platform's AI-powered comparisons can help you identify the most accurate and reproducible methods for your Gluconeogenesis experiments, enabling you to choose the best option and enhance the scientific discovery process. 3. PubCompare.ai streamlines your access to the latest Gluconeogenesis research, providing valuable insights that can improve the quality and reproducibility of your experiments.

Gluconeogenesis is the metabolic process that generates glucose from non-carbohydrate precursors, such as amino acids, lactate, and glycerol.
This crucial pathway helps maintain blood glucose levels during periods of fasting or starvation.
PubCompare.ai, an innovative AI-driven platform, can optimize your Gluconeogenesis research by quickly locating relevant protocols from literature, preprints, and patents, while utilizing AI-powered comparisons to identify the most accurate and reproducible methods.
Enhance your scientific discovery process with this powerful tool that streamlines access to the latest Gluconeogenesis research and provides valuable insights to improve your experiments.

Most cited protocols related to «Gluconeogenesis»

Telomere Dynamics and Mitochondrial Function

Terc^−/− and Tert^−/−, p53^−/− mice have been described previously^{15 (link),44 (link)}. Microarray analysis of HSCs, heart and liver tissues from WT, G1 and G4 Tert^−/− and G2 Terc^−/− mice was performed using either SAM (liver and heart) or fold change differences (HSCs) followed by Ingenuity pathway analysis (IPA). Quantitative RT–qPCR was analysed by ΔΔCt method. qPCR-based mitochondrial quantification was performed with two different primer sets for genomic and mitochondrial loci. Shock-frozen heart and liver tissues were used for ATP determination by HPLC. Mitochondrial oxygen consumption studies were performed in isolated heart and liver mitochondria using a XF24 extracellular flux analyser with substrates feeding electrons into complexes I, II and IV. Murine transthoracic echocardiography was conducted using a high-resolution micro ultrasound system as described previously^{45 (link)}. Competitive transplant experiments were performed following standard protocols. Fasting glucose concentrations were determined after 12–16 h of fasting. For in vivo Ad-Tert/PGC-1α transduction studies, mice were transduced with 10⁹ virus particles per mouse and peripheral glucose levels determined 5–6 days post infection. Gluconeogenesis in isolated hepatocytes was determined following established protocols and glucose concentration is reported after protein standardization^{24 (link)}. For p53–ER activation studies in MEFs, control or experimental cells were either treated with ethanol vehicle or 4-OHT and mitochondrial mass was determined by MitoGreen and by qPCR. For promoter analysis, sequences of 2.8 kb (PGC-1α) and 2.6 kb (PGC-1β), upstream of the start sites, were amplified by PCR from genomic mouse heart DNA and cloned into a luciferase reporter vector. Upstream lengths were chosen based on potential p53 binding sites as identified by TRANSFAC. For chromatin immunoprecipitation, we followed the EZ-Chip protocol (Promega) using p53 specific antibody and control IgG. Doxorubicin was administered at 7.5 mg per kg body weight into 8-week-old mice and echocardiography was performed 7 days later. For full details, see Supplementary Methods.

Sahin E., Colla S., Liesa M., Moslehi J., Müller F.L., Guo M., Cooper M., Kotton D., Fabian A.J., Walkey C., Maser R.S., Tonon G., Foerster F., Xiong R., Wang Y.A., Shukla S.A., Jaskelioff M., Martin E.S., Heffernan T.P., Protopopov A., Ivanova E., Mahoney J.E., Kost-Alimova M., Perry S.R., Bronson R., Liao R., Mulligan R., Shirihai O.S., Chin L, & DePinho R.A. (2011). Telomere dysfunction induces metabolic and mitochondrial compromise. Nature, 470(7334), 359-365.

Publication 2011

afimoxifene Binding Sites Body Weight Cells Cloning Vectors DNA Chips Doxorubicin Echocardiography Electrons Ethanol Freezing Genome Gluconeogenesis Glucose Heart Hepatocyte High-Performance Liquid Chromatographies Immunoglobulins Immunoprecipitation, Chromatin Infection Liver Luciferases Microarray Analysis Mitochondria Mitochondria, Liver Mus NADH Dehydrogenase Complex 1 Oligonucleotide Primers Oxygen Consumption PPARGC1A protein, human Promega Proteins Shock, Cardiogenic Stem Cells, Hematopoietic telomerase RNA component TERT protein, human Tissues Transplantation Ultrasonography Virion

Comprehensive Metabolic Profiling of Offspring

A comprehensive profiling of offspring circulating lipids, lipoproteins, and metabolites was done by a high-throughput NMR metabolomics platform, providing a snapshot of offspring serum metabolome at follow-up [20 (link),21 (link)]. In ALSPAC, offspring metabolic traits were assessed on fasting (minimum 6 hours) plasma at 2 ages (mean ages of 15.5 and 17.8), and we used data from either of these. As we were interested in lasting effects into reproductive years, we prioritised measures from the older age follow-up and used the earlier measures only for participants who did not have measures at mean age 17.8. Mean age at assessment in the whole cohort after using both time points was 17. Participants of both NFBCs fasted overnight before serum collection on the morning of clinic attendance (8 to 11 AM) at mean age 16 (NFBC86) and 31 (NFBC66) years.
Collectively, the 153 metabolic traits measured by the platform represent a broad molecular signature of systemic metabolism [20 (link),21 (link)]. The platform provided simultaneous quantification of lipoprotein lipids and subclasses, FAs and FA compositions, ketone bodies, amino acids, as well as glycolysis and gluconeogenesis-related metabolites in absolute concentration units. This platform has been applied in various large-scale epidemiological and genetic studies [22 (link)–25 (link)]; the detailed protocol, including information on quality control, has been published elsewhere [21 (link),26 (link)] and more information is given in S1 Text.

Santos Ferreira D.L., Williams D.M., Kangas A.J., Soininen P., Ala-Korpela M., Smith G.D., Jarvelin M.R, & Lawlor D.A. (2017). Association of pre-pregnancy body mass index with offspring metabolic profile: Analyses of 3 European prospective birth cohorts. PLoS Medicine, 14(8), e1002376.

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Publication 2017

Amino Acids Biological Markers Birth Gluconeogenesis Glycolysis Ketone Bodies Lipid A Lipids Lipoproteins Metabolism Metabolome Plasma Reproduction Serum

Quantifying Hepatic Metabolic Pathways

A detailed experimental section is available online. Primary hepatocytes were isolated by collagenase perfusion as described previously^{29 (link)}. Adenine nucleotides were extracted from cells and liver with perchloric acid and measured by ion pair RP-HPLC. cAMP in primary hepatocytes and frozen liver tissue was measured by ELISA (GE Healthcare) using the manufacturer’s lysis buffer. PKA activity was assayed in cell lysates as PKI sensitive Kemptide phosphorylation. PKA-FRET activity probes were used to examine intracellular PKA activity on a spinning disc confocal microscope^{16 (link)}. Adenylyl Cyclase assays were performed using Adenosine-5′-triphosphate [α-³²P] (American Radiolabeled Chemicals) and quantifying cAMP as previously described^{30 (link)}. Glucose output studies in primary hepatocytes from fasted mice were carried out in Krebs buffer containing gluconeogenic substrates (20 mM lactate, 2 mM pyruvate, 10 mM glutamine) and were quantified using hexokinase based glucose assays (Sigma). For in vivo experiments metformin was gavaged at the indicated dosage and glucagon was injected intraperitoneally at the indicated dosages. Tissues were collected rapidly from anesthetized mice and frozen in precooled metal clamps. All results are expressed as the mean ± SEM. All two group comparisons were deemed statistically significant by unpaired 2 tailed student’s t-test if p<0.05.

Miller R.A., Chu Q., Xie J., Foretz M., Viollet B, & Birnbaum M.J. (2013). Biguanides suppress hepatic glucagon signaling by decreasing production of cyclic AMP. Nature, 494(7436), 256-260.

Publication 2012

Adenine Nucleotides Adenosine Triphosphate Adenylate Cyclase Biological Assay Buffers Cells Collagenase Enzyme-Linked Immunosorbent Assay Fluorescence Resonance Energy Transfer Freezing Glucagon Gluconeogenesis Glucose Glutamine Hepatocyte Hexokinase High-Performance Liquid Chromatographies kemptide Lactate Liver Metals Metformin Mus Perchloric Acid Perfusion Phosphorylation Protoplasm Pyruvate Student Tissues

Quantifying Hepatic Metabolic Pathways

Miller R.A., Chu Q., Xie J., Foretz M., Viollet B, & Birnbaum M.J. (2013). Biguanides suppress hepatic glucagon signaling by decreasing production of cyclic AMP. Nature, 494(7436), 256-260.

Publication 2012

Embryonic Glucose Quantification Protocol

Protocol full text hidden due to copyright restrictions

Open the protocol to access the free full text link

Publication 2010

Biological Assay Body Size Buffers Centrifugation Dry Ice Embryo Enzymes Fluorescence Freezing Gluconeogenesis Glucose Glycolysis Horseradish Peroxidase Hyperostosis, Diffuse Idiopathic Skeletal Institutional Animal Care and Use Committees Mus Oxidase, Glucose Zebrafish

Most recents protocols related to «Gluconeogenesis»

Potentiation of Gluconeogenesis by LbNOX

Not available on PMC !

Example 6

As a result of its ability to elevate the intracellular ratio of NAD⁺ to NADH, LbNOX is also capable of potentiating gluconeogenesis in mammalian cells (e.g., human cells). The first step of gluconeogenesis from lactate is the conversion of lactate to pyruvate, which requires cytosolic NAD⁺. Gluconeogenesis from lactate was significantly increased when primary hepatocytes were transduced with either LbNOX or mitoLbNOX-containing adenovirus (FIG. 3D). The effect of LbNOX and mitoLbNOX on gluconeogenesis was commensurate to their effect on lactate/pyruvate ratio (FIG. 3B), suggesting that cytoplasmic and not mitochondrial NAD⁺/NADH is important for regulation of gluconeogenesis rate from lactate. These examples demonstrate the ability of water-forming NADH oxidases to control the rate of gluconeogenesis upon introducing these enzymes to mammalian cells.

US11866736B2. Protein prostheses for mitochondrial diseases or conditions (2024-01-09). The General Hospital Corporation [US]. Inventors: Vamsi Mootha [US], Denis Titov [US], Valentin Cracan [US], Zenon Grabarek [US].

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Patent 2024

Adenovirus Vaccine Cells Cytoplasm Cytosol Enzymes Gluconeogenesis Hepatocyte Homo sapiens Lactates Mammals Mitochondria NADH Protoplasm Pyruvates Water-Splitting Enzyme of Photosynthesis

Quantifying Metabolic Flux Dynamics

The calculation follows the method as prior reported (50 ). Briefly, for a metabolite with carbon number

C

, the labeled isotopologue is noted as

[M + i]

, and its fraction is noted as

L_{[M + i]}

, with

i

being the number of ¹³C atoms in the isotopologue. The overall ¹³C labeling

L_{metabolite}

of the metabolite is calculated as the weighted average of atomized labeling of all isotopologues, or mathematically,

L_{metabolite} = \sum_{i = o}^{n} \frac{i}{C} L_{[M + i]}

The normalized labeling

L_{m e t a b o l i t e \leftarrow t r a c e r}

is defined as the labeling of a metabolite normalized by the labeling of the infused tracer, as

L_{m e t a b o l i t e \leftarrow t r a c e r} = \frac{L_{metabolite}}{L_{tracer}}

As such, the direct contribution of gluconeogenic substrates to glucose production is algebraically calculated by solving the matrix equation

[\begin{matrix} 1 & L_{g l y \leftarrow l a c} & L_{a l a \leftarrow l a c} \\ L_{l a c \leftarrow g l y} & 1 & L_{a l a \leftarrow g l y} \\ L_{l a c \leftarrow a l a} & L_{g l y \leftarrow a l a} & 1 \end{matrix}] [\begin{matrix} f_{lac} \\ f_{gly} \\ f_{ala} \end{matrix}] = [\begin{matrix} L_{g l u \leftarrow l a c} \\ L_{g l u \leftarrow g l y} \\ L_{g l u \leftarrow a l a} \end{matrix}]

Specifically, let

M

be the matrix and

f

the vector on the left side, and

L

the vector on the right side. The operation seeks to

\begin{matrix} m i n ∥M \cdot f - L∥, s u b j e c t t o v e c t o r f \geq v e c t o r 0 \end{matrix}

The equation is solved using the R package limSolve (51 ). The error was estimated using Monte Carlo simulation by running the matrix equation 100 times, each time using randomly sampled

L_{m e t a b o l i t e \leftarrow t r a c e r}

values drawn from a normal distribution based on the mean and SE of entries in

M

and

f

. The calculated

f

's were pooled to calculate the error. This scheme was extended to calculate the mutual interconversions among the metabolites. The peak intensity of each measured isotope was corrected by natural abundance. To calculate the fraction of ¹³C-labeled carbon atoms of glucose, pyruvate, lactate, glutamine, and alanine derived from ¹³C-glucose and ¹³C-lactate, percent ¹³C enrichment (%) was first calculated from the data corrected by natural abundance and then normalized based on the serum tracer enrichment.

Yook J.S., Taxin Z.H., Yuan B., Oikawa S., Auger C., Mutlu B., Puigserver P., Hui S, & Kajimura S. (2023). The SLC25A47 locus controls gluconeogenesis and energy expenditure. Proceedings of the National Academy of Sciences of the United States of America, 120(9), e2216810120.

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Publication 2023

Alanine Carbon Cloning Vectors Gluconeogenesis Glucose Glutamine Isotopes Lactates Pyruvate Serum

Modeling Glucose Dynamics during Physical Activity

Glucose demand by active muscles increases acutely during PA and glucose uptake from plasma is upregulated. Simultaneously, hepatic glucose production by gluconeogenesis and glycogenolysis increases to maintain plasma glucose levels [37 (link)]. These processes are linear in PA intensity [17 (link)]. We therefore define the insulin-independent rise in GU (r_GU [1/min]) and GP (r_GP [1/min]) rates as

\begin{matrix} \begin{matrix} \frac{d r_{G U} (t)}{d t} & = & q_{1} \cdot f (Y (t); a_{Y}, n_{1}) \cdot Y (t) - q_{2} \cdot r_{G U} (t) \\ \frac{d r_{G P} (t)}{d t} & = & q_{3} \cdot f (Y (t); a_{Y}, n_{1}) \cdot Y (t) - q_{4} \cdot r_{G P} (t), \end{matrix} \end{matrix}

where q_i are rate parameters.

Deichmann J., Bachmann S., Burckhardt M.A., Pfister M., Szinnai G, & Kaltenbach H.M. (2023). New model of glucose-insulin regulation characterizes effects of physical activity and facilitates personalized treatment evaluation in children and adults with type 1 diabetes. PLOS Computational Biology, 19(2), e1010289.

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Publication 2023

Gluconeogenesis Glucose Glycogenolysis Insulin Muscle Tissue Plasma

Modeling Glycogen Depletion and Glucose Regulation

Liver glycogen stores may deplete during prolonged PA and GP cannot be maintained by gluconeogenesis alone, causing an accelerated drop in glucose levels [7 (link), 38 (link)]. We follow Roy et al. [17 (link)] and assume that glycogen stores deplete in proportion to exercise intensity and duration. The time t_depl [min] to depletion determined from the integrated AC count and PA duration is then given by:

\begin{matrix} t_{d e p l} (t) = - a_{d e p l} \cdot \frac{P A_{i n t} (t)}{t_{P A} (t)} + b_{d e p l} . \end{matrix}

After depletion sets in, we allow a drop in GP rate, r_depl [1/min], defined by

\begin{matrix} \begin{matrix} \frac{d r_{d e p l} (t)}{d t} & = & q_{6} \cdot [f (t_{P A} (t); t_{d e p l}, n_{1}) \cdot r_{m} (t) - r_{d e p l} (t)] \\ r_{m} (t) & = & β \cdot (\frac{q_{3}}{q_{4}} \cdot Y (t) + r_{G P b}), \end{matrix} \end{matrix}

where the transfer function f(t_PA; t_depl, n₁) indicates whether exercise time exceeds t_depl and q₆ is a rate parameter. The maximum decrease r_m [1/min] in GP is the sum of the basal resting GP rate, r_GPb, and the PA-driven GP rate at steady state, q₃/q₄ ⋅ Y(t), scaled by the proportion of net hepatic glucose production attributed to glycogenolysis, β.

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Publication 2023

Gluconeogenesis Glucose Glycogen Glycogenolysis Liver Glycogen

Comprehensive Gene Expression Analysis of Metabolic Pathways

For cDNA synthesis, 1000 ng of intact RNA was reversed to cDNA with a reverse transcription kit (YEASEN, Shanghai, China) with the concentration detected. The synthesized cDNA was diluted to 200 ng/μL as a template for RT-qPCR. To detect carbohydrate metabolism, the expression of genes related to glycogen synthesis (ugp2b, gys2), glycogen degradation (pygl), gluconeogenesis (pck1, pcxb), glycolysis (gck), TCA cycle pathway (idh), and pentose phosphate pathway (g6pd) were evaluated. The expression of genes related to lipid synthesis (fasn, acaca, aclyb) and decomposition (acadl, acaa1, lpl) were determined to illustrate the influence on lipid metabolism, and the expression of genes related to the urea cycle (gs, cps3, otc, ass, asl, and arg1) was also detected. The qPCR was performed in Jena qTOWER3G system using the real-time quantitative PCR detection kit EvaGreen 2 × qPCR Master mix (YEASEN, Shanghai, China): pre-denaturation at 95 °C for 5 min; denaturation at 95 °C for 10 s; annealing and extension at 60 °C for 30 s; and PCR reaction step running 40 cycles. After RT-qPCR, melting curves were analyzed to ensure the specificity of the reaction. Using 18s as the internal reference gene, the relative quantitative data analysis was performed by the 2^−ΔΔCt method. RT-qPCR data were analyzed using GraphPad Prism 6. The primers used in the present study are shown in Table 1.

Zou J., Hu P., Wang M., Chen Z., Wang H., Guo X., Gao J, & Wang Q. (2023). Liver Injury and Metabolic Dysregulation in Largemouth Bass (Micropterus salmoides) after Ammonia Exposure. Metabolites, 13(2), 274.

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Publication 2023

ACACA protein, human Anabolism arginase-1, human Carbohydrate Metabolism Citric Acid Cycle DNA, Complementary FASN protein, human Gene Expression Genes Gluconeogenesis Glucosephosphate Dehydrogenase Glycogen Glycogenolysis Glycolysis Lipid Metabolism Lipogenesis Oligonucleotide Primers Pentose Phosphate Pathway prisma Real-Time Polymerase Chain Reaction Reverse Transcription Urea

Top products related to «Gluconeogenesis»

Sodium pyruvate by Merck Group

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Sodium pyruvate is a chemical compound that functions as an energy source and metabolic intermediate in cell culture media. It is commonly used as a supplement in cell culture applications to support cell growth and metabolism.

Glucose assay kit by Merck Group

Sourced in United States, China, Switzerland, France, Germany, Sao Tome and Principe

The Glucose assay kit is a laboratory instrument designed to quantify the concentration of glucose in a sample. It measures the amount of glucose present through a colorimetric or fluorometric reaction, providing an accurate and reliable analysis.

Glucose go assay kit by Merck Group

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The Glucose (GO) Assay Kit is a laboratory equipment product designed to measure the concentration of glucose in a sample. It utilizes the glucose oxidase (GO) enzyme to catalyze the oxidation of glucose, which is then detected and quantified colorimetrically. The kit provides a simple, accurate, and rapid method for determining glucose levels in a variety of biological samples.

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High capacity cdna reverse transcription kit by Thermo Fisher Scientific

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Rabbit anti gk antibody by LifeSpan BioSciences

The Rabbit anti-GK antibody is a primary antibody that recognizes the Glucokinase (GK) protein. GK is an enzyme involved in glucose metabolism and is commonly used as a marker in biological research. This antibody can be used for the detection and analysis of GK expression in various samples and applications.

Goat anti pfk1 by GenWay Biotech

Goat anti-PFK1 is a primary antibody that binds to and detects Phosphofructokinase 1 (PFK1), an essential enzyme involved in glycolysis. This antibody can be used in various immunoassay applications for the identification and quantification of PFK1.

Mouse anti ampk by Cell Signaling Technology

Mouse anti-AMPK is a laboratory reagent that can be used to detect the presence and measure the levels of the AMPK (AMP-activated protein kinase) protein in biological samples. AMPK is an enzyme that plays a crucial role in the regulation of cellular energy homeostasis. This antibody can be used in various immunological techniques, such as Western blotting, immunoprecipitation, and immunohistochemistry, to study the expression and activity of AMPK in different cell types and tissues.

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Rabbit anti-Shc is a primary antibody that recognizes the Shc (Src homology 2 domain-containing) protein. Shc is an important adaptor protein involved in various cellular signaling pathways. The rabbit anti-Shc antibody can be used to detect and study the expression and distribution of Shc in biological samples.

What is the purpose of Gluconeogenesis?

How can PubCompare.ai help with Gluconeogenesis research?

PubCompare.ai is an innovative AI-driven platform that can optimize your Gluconeogenesis research in several ways: 1. It allows you to screen protocol literature more efficiently, helping you quickly locate relevant protocols from literature, preprints, and patents. 2. The platform's AI-powered comparisons can help you identify the most accurate and reproducible methods for your Gluconeogenesis experiments, enabling you to choose the best option and enhance the scientific discovery process. 3. PubCompare.ai streamlines your access to the latest Gluconeogenesis research, providing valuable insights that can improve the quality and reproducibility of your experiments.

More about "Gluconeogenesis"

Gluconeogenesis is the metabolic process that generates glucose from non-carbohydrate precursors, such as amino acids, lactate, and glycerol.
This crucial pathway, also known as glucose synthesis or glyconeogenesis, helps maintain blood glucose levels during periods of fasting or starvation.
Sodium pyruvate is a common gluconeogenic substrate, which can be converted to glucose through the gluconeogenic pathway.
Glucose assay kits, such as the Glucose (GO) Assay Kit (GAGO20), can be used to measure glucose levels and evaluate gluconeogenic activity.
The High-Capacity cDNA Reverse Transcription Kit can be employed to study the expression of genes involved in gluconeogenesis, like the key enzymes phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase).
Antibodies targeting glucokinase (GK), phosphofructokinase-1 (PFK1), and AMP-activated protein kinase (AMPK) can provide insights into the regulation of gluconeogenesis.
PubCompare.ai, an innovative AI-driven platform, can optimize your Gluconeogenesis research by quickly locating relevant protocols from literature, preprints, and patents, while utilizing AI-powered comparisons to identify the most accurate and reproducible methods.
This powerful tool streamlines access to the latest Gluconeogenesis research and provides valuable insights to improve your experiments, enhancing your scientific discovery process.
Explore how PubCompare.ai can help you advance your Gluconeogenesis studies and uncover new findings.
Leverage this AI-powered platform to access a wealth of information, compare research methods, and optimize your experimental design for more reliable and impactful results.