ArticleDiabetologia2006
Anaplerosis via pyruvate carboxylase is required for the fuel-induced rise in the ATP:ADP ratio in rat pancreatic islets.
Article in Diabetologia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 71 citations in OpenAlex.
- Identification of eight genomic protective alleles for mitochondrial diabetes by Kinship-graph convolutional network.Journal of diabetes investigation · 2024Article
- Mechanisms controlling pancreatic islet cell function in insulin secretion.Nature reviews. Molecular cell biology · 2021Review
- Augmented mitochondrial energy metabolism is an early response to chronic glucose stress in human pancreatic beta cells.Diabetologia · 2020Article
- Pyruvate Kinase Controls Signal Strength in the Insulin Secretory Pathway.Cell metabolism · 2020Article
- Review
- Article
- Y1 receptor deficiency in β-cells leads to increased adiposity and impaired glucose metabolism.Scientific reports · 2018Article
- Metabolic activation-driven mitochondrial hyperpolarization predicts insulin secretion in human pancreatic beta-cells.Biochimica et biophysica acta. Bioenergetics · 2018Article
- Cell cycle-related metabolism and mitochondrial dynamics in a replication-competent pancreatic beta-cell line.Cell cycle (Georgetown, Tex.) · 2017Article
- L-cysteine reversibly inhibits glucose-induced biphasic insulin secretion and ATP production by inactivating PKM2.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Mitochondrial metabolism of pyruvate is essential for regulating glucose-stimulated insulin secretion.The Journal of biological chemistry · 2014Article
- Control of voltage-gated potassium channel Kv2.2 expression by pyruvate-isocitrate cycling regulates glucose-stimulated insulin secretion.The Journal of biological chemistry · 2013Article
- Exercise training enhances rat pancreatic islets anaplerotic enzymes content despite reduced insulin secretion.European journal of applied physiology · 2011Article
- Reduced cytochrome C is an essential regulator of sustained insulin secretion by pancreatic islets.The Journal of biological chemistry · 2011Article
- Article
- Tight coupling between glucose and mitochondrial metabolism in clonal beta-cells is required for robust insulin secretion.The Journal of biological chemistry · 2009Article
- Glutaredoxin-1 mediates NADPH-dependent stimulation of calcium-dependent insulin secretion.Molecular endocrinology (Baltimore, Md.) · 2009Article
- Prospects for clinical cancer metabolomics using stable isotope tracers.Experimental and molecular pathology · 2009Review
- Metabolic cycling in control of glucose-stimulated insulin secretion.American journal of physiology. Endocrinology and metabolism · 2008Review
- The role of pyruvate carboxylase in insulin secretion and proliferation in rat pancreatic beta cells.Diabetologia · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisThe molecular mechanisms of insulin release are only partially known. Among putative factors for coupling glucose metabolism to insulin secretion, anaplerosis has lately received strong support. The anaplerotic enzyme pyruvate carboxylase is highly expressed in beta cells, and anaplerosis influences insulin secretion in beta cells. By inhibiting pyruvate carboxylase in rat islets, we aimed to clarify the hitherto unknown metabolic events underlying anaplerotic regulation of insulin secretion.
methodsPhenylacetic acid (5 mmol/l) was used to inhibit pyruvate carboxylase in isolated rat islets, which were then assessed for insulin secretion, fuel oxidation, ATP:ADP ratio, respiration, mitochondrial membrane potential, exocytosis and ATP-sensitive K(+) channel (K(ATP)-channel) conductance.
resultsWe found that the glucose-provoked rise in ATP:ADP ratio was suppressed by inhibition of pyruvate carboxylase. In contrast, fuel oxidation, respiration and mitochondrial membrane potential, as well as Ca(2+)-induced exocytosis and K(ATP)-channel conductance in single cells, were unaffected. Insulin secretion induced by alpha-ketoisocaproic acid was suppressed, whereas methyl-succinate-stimulated secretion remained unchanged. Perifusion of rat islets revealed that inhibition of anaplerosis decreased both the second phase of insulin secretion, during which K(ATP)-independent actions of fuel secretagogues are operational, as well as the first and K(ATP)-dependent phase. CONCLUSIONS/
interpretationOur results are consistent with the concept that anaplerosis via pyruvate carboxylase determines pyruvate cycling, which has previously been shown to correlate with glucose responsiveness in clonal beta cells. These processes, controlled by pyruvate carboxylase, seem crucial for generation of an appropriate ATP:ADP ratio, which may regulate both phases of fuel-induced insulin secretion.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.