ArticleMedicine and science in sports and exercise2011
Postexercise skeletal muscle glucose transport is normal in kininogen-deficient rats.
Article in Medicine and science in sports and exercise, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 11 citations in OpenAlex.
- Bradykinin, insulin, and glycemia responses to exercise performed above and below lactate threshold in individuals with type 2 diabetes.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017Trial
- Genetic reduction of skeletal muscle glycogen synthase 1 abundance reveals that the refeeding-induced reversal of elevated insulin-stimulated glucose uptake after exercise is not attributable to achieving a high muscle glycogen concentration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Angiotensin-(1-7) Participates in Enhanced Skeletal Muscle Insulin Sensitivity After a Bout of Exercise.Journal of the Endocrine Society · 2020Article
- Fiber type-selective exercise effects on AS160 phosphorylation.American journal of physiology. Endocrinology and metabolism · 2019Article
- Postexercise improvement in glucose uptake occurs concomitant with greater γ3-AMPK activation and AS160 phosphorylation in rat skeletal muscle.American journal of physiology. Endocrinology and metabolism · 2018Article
- Serum Is Not Necessary for Prior Pharmacological Activation of AMPK to Increase Insulin Sensitivity of Mouse Skeletal Muscle.International journal of molecular sciences · 2018Article
- Mechanisms for greater insulin-stimulated glucose uptake in normal and insulin-resistant skeletal muscle after acute exercise.American journal of physiology. Endocrinology and metabolism · 2015Review
- Sustained postexercise increases in AS160 Thr642 and Ser588 phosphorylation in skeletal muscle without sustained increases in kinase phosphorylation.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledA single exercise bout stimulates skeletal muscle glucose transport (GT) in the absence or presence of insulin. It has been suggested that the kallikrein-kinin system may contribute to exercise effects on both insulin-independent and insulin-dependent GT. Plasma kininogen, a key kallikrein-kinin system component, is a protein substrate for the enzyme kallikrein and the source of the peptide bradykinin. PURPOSE: This study aimed to determine whether the postexercise (PEX) increase in insulin-dependent or insulin-independent GT is reduced in rats deficient in plasma kininogen versus normal rats.
methodsMale Brown Norway (BN) and Brown Norway Katholiek (BNK; plasma kininogen-deficient) rats were studied. BN and BNK rats were assigned to exercise (4×30-min swim) or sedentary (SED) groups. Rats were anesthetized immediately (0hPEX) or 3 h (3hPEX) after exercise. For 0hPEX and 0hSED rats, one epitrochlearis muscle per rat was used for AMPK phosphorylation and muscle glycogen analyses. The contralateral muscle was incubated with [H]-3-O-methylglucose (3-MG) for GT assay. For 3hPEX and 3hSED rats, one muscle from each rat was incubated without insulin, and the contralateral muscle was incubated with 60 μU·mL insulin, and both muscles were incubated with 3-MG for GT measurement.
resultsFor 0hPEX versus 0hSED, both BN and BNK rats had greater insulin-independent GT and AMPK phosphorylation with reduced glycogen after exercise. No genotype effects were found 0hPEX. There was a significant main effect of exercise (3hPEX>3hSED) and no interaction between exercise and genotype for basal or insulin-stimulated GT.
conclusionsPlasma kininogen deficiency did not alter insulin-independent GT, AMPK phosphorylation, or glycogen depletion 0hPEX or insulin-dependent GT 3hPEX, suggesting that normal plasma kininogen is not essential for these important exercise effects.
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.