Rapamycin-Induced Glucose Intolerance: Hunger or Starvation Diabetes
Open accessAbstract
Rapamycin prolongs healthy lifespan in yeast, flies and mammals and delays age-related diseases, including cancer and atherosclerosis. Rapamycin is considered for prevention of diabetic complications, such as retinopathy and nephropathy, and acute treatment with rapamycin decreases insulin resistance. However, under certain conditions, chronic administration of rapamycin may cause glucose intolerance and even provoke type II diabetes. This does not fit logically with its potential effects against diabetic complications. This also seems puzzling, because calorie restriction (CR) can prevent type II diabetes and its complications, and rapamycin mimics CR. It was somehow forgotten that almost two centuries ago, Claude Bernard discovered "starvation diabetes," as shown later, characterized by glucose intolerance, decreased insulin, increased lipoproteins and ketones, gluconeogenesis and hepatic resistance to insulin. This reversible condition is not true diabetes: it does not lead to diabetic complications, and CR extends healthy lifespan. If rapamycin is a CR-mimetic, no wonder it may, in certain models, induce "hunger diabetes." But will rapamycin prevent true type II diabetes? Here are some answers.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Blagosklonny argued that the metabolic side effects of rapamycin are a consequence of it acting as a CRM and are required to mediate its positive effects on lifespan.
“Blagosklonny argued that the metabolic side effects of rapamycin are a consequence of it acting as a CRM and are required to mediate its positive effects on lifespan (226).”
From A Critical Review of the Evidence That Metformin Is a Putative Anti-Aging Drug That Enhances Healthspan and Extends Lifespan (2021) · cites this paper as [226]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Cites
The publisher hasn’t deposited this paper’s reference list.
Part of this paper’s reference list could not be split into single entries.
Research works printed but not linked: 7
- Tremblay F, Marette A. Amino acid and insulin signaling via the mTOR/p70 S6 kinase pathway. A negative feedback mechanism leading to insulin resistance in skeletal muscle cells. J Biol Chem 2001; 276:38052-60; PMID:11498541.
- Haruta T, Uno T, Kawahara J, Takano A, Egawa K, Sharma PM, et al. A rapamycin-sensitive pathway downregulates insulin signaling via phosphoryla- tion and proteasomal degradation of insulin recep- tor substrate-1. Mol Endocrinol 2000; 14:783-94; PMID:10847581; http://dx.doi.org/10.1210/ me.14.6.783. · DOI
- Blagosklonny MV. Insulin resistance, complications, diabetes and mTOR: Surprising sequence of events and therapeutic opportunities. Aging 2011; 3; In press.
- Colagiuri S, Lee CM, Wong TY, Balkau B, Shaw JE, Borch-Johnsen K. Glycemic thresholds for diabetes- specific retinopathy: implications for diagnostic cri- teria for diabetes. Diabetes Care 2011; 34:145-50; PMID:20978099; http://dx.doi.org/10.2337/dc10- 1206. · DOI · Paper page
- Meigs JB, D'Agostino RBS, Nathan DM, Rifai N, Wilson PW. Longitudinal association of gly- cemia and microalbuminuria: the Framingham Offspring Study. Diabetes Care 2002; 25:977-83; PMID:12032102; http://dx.doi.org/10.2337/dia- care.25.6.977. · DOI
- Barbour LA, McCurdy CE, Hernandez TL, Friedman JE. Chronically increased S6K1 is associat- ed with impaired IRS1 signaling in skeletal muscle of GDM women with impaired glucose tolerance post- partum. J Clin Endocrinol Metab 2011; 96:1431- 41; PMID:21289241; http://dx.doi.org/10.1210/ jc.2010-116. · DOI
- Chiasson JL, Rabasa-Lhoret R. Prevention of type 2 diabetes: insulin resistance and beta-cell function. Diabetes 2004; 53:34-8; PMID:15561919; http:// dx.doi.org/10.2337/diabetes.53.suppl_3.S34. · DOI
Cited by
Sorted by citations
López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013) · Cell · doi:10.1016/j.cell.2013.05.039 · Cited by 14,982 · see citing works
“Interventions using chemical inducers of macroautophagy (another type of autophagy different than chaperonemediated autophagy) have spurred extraordinary interest after the discovery that constant or intermittent administration of the mTOR inhibitor rapamycin can increase the lifespan of middleaged mice (Blagosklonny,…”
BackgroundThe Mechanistic Links Between Proteasome Activity, Aging and Agerelated Diseases
Sáez, I., & Vı́lchez, D. (2014) · Current Genomics · doi:10.2174/138920291501140306113344 · Cited by 318 · see citing works
“Interestingly, administration of rapamycin, an autophagy inducer, considerably delays aging in mice and other models [74-76].”
BackgroundMohammed, I., Hollenberg, M. D., Ding, H., & Triggle, C. R. (2021) · Frontiers in Endocrinology · doi:10.3389/fendo.2021.718942 · Cited by 278 · see citing works
Blagosklonny, M. V. (2012) · Aging · doi:10.18632/aging.100443 · Cited by 251 · see citing works
“Examples include beta-cell failure [115], ovarian failure (menopause) [116], myocardial infarction, stroke, renal failure, broken hips, cancer metastases and so on [6, 117].”
BackgroundSelf-citationYang, S.-B., Tien, A.-C., Boddupalli, G., Xu, A. W., Jan, Y. N., & Jan, L. Y. (2012) · Neuron · doi:10.1016/j.neuron.2012.03.043 · Cited by 242 · see citing works
“Depending on the dosage and duration, rapamycin may affect glucose homeostasis in different ways (Blagosklonny, 2011b).”
BackgroundRapamycin for longevity: opinion article
Blagosklonny, M. V. (2019) · Aging · doi:10.18632/aging.102355 · Cited by 210 · see citing works
“It is not completely clear why SPD was observed in only some studies and was not observed in other studies (see for references [38, 73]).”
BackgroundInfluentialSelf-citationAnswering the ultimate question “What is the Proximal Cause of Aging?”
Blagosklonny, M. V. (2012) · Aging · doi:10.18632/aging.100525 · Cited by 191 · see citing works
Self-citationXenohormetic and anti-aging activity of secoiridoid polyphenols present in extra virgin olive oil
Menéndez, J. A., Joven, J., Aragonès, G., Barrajón‐Catalán, E., Beltrán‐Debón, R., Borrás‐Linares, I., Camps, J., Corominas-Faja, B., Cufí, S., Fernández‐Arroyo, S., et al. (2013) · Cell Cycle · doi:10.4161/cc.23756 · Cited by 150 · see citing works
Testa, G., Biasi, F., Poli, G., & Chiarpotto, E. (2014) · Current Pharmaceutical Design · doi:10.2174/13816128113196660699 · Cited by 148 · see citing works
“[433] Blagosklonny MV.”
Blagosklonny, M. V. (2013) · Cell Death and Disease · doi:10.1038/cddis.2013.506 · Cited by 116 · see citing works
“In fact, starvation, fasting and calorie restriction do not cause ‘diabetes complications’ such as neuropathy or retinopathy or atherosclerosis.(125,126) In contrast, calorie restriction prevents diabetes and diabetic complications and extends life span.”
BackgroundInfluentialSelf-citationOxidative Stress, Mitochondrial Dysfunction and the Mitochondria Theory of Aging
Kong, Y., Trabucco, S. E., & Zhang, H. (2014) · Interdisciplinary topics in gerontology and geriatrics · doi:10.1159/000358901 · Cited by 112 · see citing works
Towards natural mimetics of metformin and rapamycin
Aliper, A. M., Jellen, L. C., Cortese, F., Artemov, A. V., Karpinsky‐Semper, D., Moskalev, A., Swick, A. G., & Zhavoronkov, A. A. (2017) · Aging · doi:10.18632/aging.101319 · Cited by 111 · see citing works
“While rapamycin-induced diabetes is argued to differ from true type II diabetes [81], rapamycin may require pairing with metformin to counter induced hyperglycemia [40].”
BackgroundProspective Treatment of Age-Related Diseases by Slowing Down Aging
Blagosklonny, M. V. (2012) · American Journal Of Pathology · doi:10.1016/j.ajpath.2012.06.024 · Cited by 107 · see citing works
Self-citationNutrient Sensing, Signaling and Ageing: The Role of IGF-1 and mTOR in Ageing and Age-Related Disease
Johnson, S. C. (2018) · Sub-cellular biochemistry/Subcellular biochemistry · doi:10.1007/978-981-13-2835-0_3 · Cited by 102 · see citing works
Dose-dependent effects of mTOR inhibition on weight and mitochondrial disease in mice
Johnson, S. C., Yanos, M. E., Bitto, A., Castanza, A. S., Gagnidze, A., González, B., Gupta, K., Hui, J., Jarvie, C., Johnson, B. M., et al. (2015) · Frontiers in Genetics · doi:10.3389/fgene.2015.00247 · Cited by 91 · see citing works
“Intolerance in this assay may reflect an altered metabolic state wherein metabolism is shifted away from glucose utilization, a state of “starvation diabetes” (Blagosklonny, 2011), where animals are not physiologically primed to deal with a sudden, non-physiological increase in blood glucose levels.”
BackgroundAutophagy regulates chlorpyrifos-induced apoptosis in SH-SY5Y cells
Park, J. H., Lee, J. E., Shin, I. C., & Koh, H. C. (2013) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2013.01.013 · Cited by 92 · see citing works
Once again on rapamycin-induced insulin resistance and longevity: despite of or owing to
Blagosklonny, M. V. (2012) · Aging · doi:10.18632/aging.100461 · Cited by 89 · see citing works
“Insulin resistance and symptoms of diabetes are observed during starvation [28] and prolong severe CR [55].”
BackgroundSelf-citationFrom rapalogs to anti-aging formula
Blagosklonny, M. V. (2017) · Oncotarget · doi:10.18632/oncotarget.18033 · Cited by 83 · see citing works
“Similarly, calorie restriction increases insulin sensitivity, whereas severe calorie restriction (starvation) decreases it [129, 245].”
BackgroundSelf-citationPrevention of Age-Related Macular Degeneration–Like Retinopathy by Rapamycin in Rats
Kolosova, N. G., Muraleva, N. A., Александровна, Ж. А., Stefanova, N. A., Фурсова, А. Ж., & Blagosklonny, M. V. (2012) · American Journal Of Pathology · doi:10.1016/j.ajpath.2012.04.018 · Cited by 80 · see citing works
Self-citationFasting and rapamycin: diabetes versus benevolent glucose intolerance
Blagosklonny, M. V. (2019) · Cell Death & Disease · doi:10.1038/s41419-019-1822-8 · Cited by 74 · see citing works
Self-citationLeontieva, O. V., Demidenko, Z. N., & Blagosklonny, M. V. (2014) · Cell Death and Disease · doi:10.1038/cddis.2014.178 · Cited by 68 · see citing works
“Such metabolic alterations strikingly resemble ‘starvation diabetes’ developed during starvation or severe caloric restriction.(49) Not co-incidentally, rapamycin is caloric restriction-mimetic, causing a beneficial condition named ‘beneficial pseudo-diabetes’.”
BackgroundSelf-citationMakki, K., Taront, S., Molendi‐Coste, O., Bouchaert, E., NEVE, B. P., Eury, E., Lobbens, S., Labalette, M., Duez, H., Staels, B., et al. (2014) · PLoS ONE · doi:10.1371/journal.pone.0092684 · Cited by 65 · see citing works
Insulin resistance in the liver: Deficiency or excess of insulin?
Bazotte, R. B., Silva, L. G., & Schiavon, F. P. M. (2014) · Cell Cycle · doi:10.4161/15384101.2014.947750 · Cited by 60 · see citing works
“However, in the acini area, the hepatocytes are exposed to a spatial biochemical gradient that influences metabolism and gene expression, so cell specialization does exist to some degree, depending on locale.(37-52) Parenchymal acini of the liver are divisible into 2 circulatory zones, based on proximity to afferent v…”
BackgroundWilson, R., Deasy, W. J., Stathis, C. G., Hayes, A., & Cooke, M. B. (2018) · Nutrients · doi:10.3390/nu10030346 · Cited by 58 · see citing works
“Reduced glucose tolerance is usually a result of lower insulin release [36], however, in the current study, insulin levels were significantly higher than the ‘obese’ controls at the end of the intervention period.”
ResultNCI's provocative questions on cancer: some answers to ignite discussion
Blagosklonny, M. V. (2011) · Oncotarget · doi:10.18632/oncotarget.432 · Cited by 51 · see citing works
“Second, mTOR overactivation can cause insulin resistance [155-159], which in turn leads to a compensatory increase in insulin levels, which can promote cancer.”
BackgroundSelf-citationLeontieva, O. V., Paszkiewicz, G., & Blagosklonny, M. V. (2012) · Aging · doi:10.18632/aging.100528 · Cited by 51 · see citing works
“However, it is exactly opposite: nutrients and obesity accelerate aging, whereas calorie restriction increases lifespan [55, 148, 149, 173-188].”
BackgroundSelf-citationRoss, C. N., Salmon, A. B., Strong, R., Fernández, E., Javors, M., Richardson, A. G., & Tardif, S. D. (2015) · Aging · doi:10.18632/aging.100843 · Cited by 51 · see citing works
“Alternatively the effect of rapamycin is thought to mimic the metabolic changes associated with starvation diabetes or Type 0 diabetes [40, 41, 42]; which is often thought to be a positive, adaptive form of metabolic changes associated with enhanced metabolic efficiency and decreased risk of true diabetes.”
About-face on the metabolic side effects of rapamycin
Salmon, A. B. (2015) · Oncotarget · doi:10.18632/oncotarget.3354 · Cited by 47 · see citing works
Obese mice on a high‐fat alternate‐day fasting regimen lose weight and improve glucose tolerance
Joslin, P. M. N., Bell, R. K., & Swoap, S. J. (2016) · Journal of Animal Physiology and Animal Nutrition · doi:10.1111/jpn.12546 · Cited by 48 · see citing works
Leontieva, O. V., Paszkiewicz, G., Demidenko, Z. N., & Blagosklonny, M. V. (2013) · Cell Death and Disease · doi:10.1038/cddis.2012.202 · Cited by 44 · see citing works
“was reported that rapamycin increases levels of triglycerides in mice and humans in part due to elevated lipolysis, which is a starvation-like side effect of rapamycin.(24,25) However, at low doses used in our study, rapamycin did not affect triglycerides levels on HFD (Figure 3d).”
BackgroundSelf-citationNakamura, S. K., Nakano, S., Miyoshi, T., Yamanouchi, K., Matsuwaki, T., & Nishihara, M. (2012) · Aging · doi:10.18632/aging.100426 · Cited by 44 · see citing works
“It was suggested that signal-resistance is a hallmark of aging/senescent cells due to chronic increase in basal activity of the mTOR pathway [32, 33, 34].”
Koschei the immortal and anti-aging drugs
Blagosklonny, M. V. (2014) · Cell Death and Disease · doi:10.1038/cddis.2014.520 · Cited by 41 · see citing works
“Claude Bernard (19th century) described that during starvation humans and dogs develop reversible starvation-diabetes.(66) If a starved animal (or human) consumes sugar, this sugar will appear in the urine, forcing water to follow (polyuria).”
BackgroundSelf-citationImpact of mTOR-I on fertility and pregnancy: state of the art and review of the literature
Framarino‐dei‐Malatesta, M., Derme, M., Manzia, T. M., et al. (2013) · Expert Review of Clinical Immunology · doi:10.1586/1744666x.2013.824243 · Cited by 41 · see citing works
Blagosklonny, M. V. (2012) · Oncotarget · doi:10.18632/oncotarget.890 · Cited by 38 · see citing works
Self-citationInsulin sensitivity in long-living Ames dwarf mice
Wiesenborn, D. S., Ayala, J. E., King, E. M., & Masternak, M. M. (2014) · AGE · doi:10.1007/s11357-014-9709-1 · Cited by 34 · see citing works
“2008) but may rather promote glucose intolerance and insulin resistance (Blagosklonny 2011).”
BackgroundSESTRINs: Emerging Dynamic Stress-Sensors in Metabolic and Environmental Health
Ro, S., Fay, J., Cyuzuzo, C. I., Jang, Y., Lee, N., Song, H., & Harris, E. N. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.603421 · Cited by 34 · see citing works
“Although mTOR inhibitors were widely used previously, efficacy and safety on cancer patients are controversial due to their side effects (Kalender et al., 2010; Blagosklonny, 2011; Din et al., 2012).”
BackgroundRejuvenating immunity: “anti-aging drug today” eight years later
Blagosklonny, M. V. (2015) · Oncotarget · doi:10.18632/oncotarget.3740 · Cited by 32 · see citing works
““Starvation or Hunger Diabetes” was well known during famine and prolonged fasting [8].”
Self-citationWestfall, S., Lomis, N., & Prakash, S. (2018) · Molecular Biotechnology · doi:10.1007/s12033-018-0119-y · Cited by 32 · see citing works
PI3Kα inhibition reduces obesity in mice
Lopez-Guadamillas, E., Muñoz‐Martín, M., Martı́nez, S., Pastor, J., Fernández-Marcos, P. J., & Serrano, M. (2016) · Aging · doi:10.18632/aging.101075 · Cited by 29 · see citing works
Cdk8 attenuates lipogenesis by inhibiting SREBP-dependent transcription in Drosophila
Li, X., Zhang, M., Liu, M., Liu, T.-H., Hemba-Waduge, R.-U.-S., & Ji, J. (2022) · Disease Models & Mechanisms · doi:10.1242/dmm.049650 · Cited by 21 · see citing works
Wang, H., Zhu, X., Shen, J., Zhao, E.-F., He, D., Shen, H., Liu, H., & Zhou, Y. (2019) · BMC Genomics · doi:10.1186/s12864-019-6089-z · Cited by 23 · see citing works
Chimenti, M. S., Tucci, P., Candi, E., Perricone, R., Melino, G., & Willis, A. E. (2013) · Cell Cycle · doi:10.4161/cc.26067 · Cited by 21 · see citing works
“A greater understanding of how these pathways are regulated and function in lymphocytes becomes increasingly important with the availability and interest in the therapeutic use of drugs that alter metabolism.(91-101) Through metabolic manipulation, it may be possible to extend survival of lymphocytes and ultimately al…”
BackgroundRecent discoveries in the cycling, growing and aging of the p53 field
McCubrey, J. A., & Demidenko, Z. N. (2012) · Aging · doi:10.18632/aging.100529 · Cited by 18 · see citing works
“As recently proposed, aging is not caused by accumulation of DNA damage but is driven by signaling pathways such as TOR [13-36].”
Rehman, A., Satyam, S. M., El‐Tanani, M., Prabhakar, S., KUMARI, R. R., Shetty, P., Mohammed, S. S. N., Nafees, Z., & Alomar, B. (2025) · Cancers · doi:10.3390/cancers17152466 · Cited by 17 · see citing works
“The chronic administration of rapamycin and its related compounds results in impaired glucose homeostasis and weakened immune responses but metformin’s insulin-sensitizing and immune-preserving effects make it suitable to extend the use of rapalogs for lifespan extension [143,144].”
The mystery of the ketogenic diet: benevolent pseudo-diabetes
Blagosklonny, M. V. (2019) · Cell Cycle · doi:10.1080/15384101.2019.1644765 · Cited by 15 · see citing works
Self-citationDoes Aging Activate T-cells to Reduce Bone Mass and Quality?
Aurora, R., & Novack, D. V. (2022) · Current Osteoporosis Reports · doi:10.1007/s11914-022-00745-8 · Cited by 12 · see citing works
mTOR inhibitors for treatment of low-risk prostate cancer
Liss, M. A., Rickborn, L., DiGiovanni, J., Bacich, D. J., deGraffenried, L. A., Parihar, M., Thompson, I. M., & Sharp, Z. D. (2018) · Medical Hypotheses · doi:10.1016/j.mehy.2018.06.004 · Cited by 12 · see citing works
Nutrition and energetics in rodent longevity research
Gibbs, V. K., & Smith, D. L. (2016) · Experimental Gerontology · doi:10.1016/j.exger.2016.04.004 · Cited by 13 · see citing works
“However, one of the more puzzling and contraindicated side effects of rapamycin treatment is the development of insulin resistance which is normally considered counterproductive to aging and disease protection (Blagosklonny, 2011; Bartke & Brown-Borg, 2004).”
BackgroundFramarino‐dei‐Malatesta, M., Derme, M., Napoli, A., Iaria, G., Manzia, T. M., Orlando, G., Casorelli, A., & Berloco, P. B. (2014) · Transplantation Proceedings · doi:10.1016/j.transproceed.2014.07.047 · Cited by 11 · see citing works
Sereno, J., Parada, B., Rodrigues‐Santos, P., et al. (2013) · Transplantation Proceedings · doi:10.1016/j.transproceed.2013.02.085 · Cited by 9 · see citing works
Peripheral tissular analysis of rapamycin’s effect as a neuroprotective agent in vivo
González-Alcocer, A., Gopar‐Cuevas, Y., Soto‐Domínguez, A., Loera‐Arias, M. D. J., Cárdenas, O. S., Montes‐de‐Oca‐Luna, R., Rodríguez‐Rocha, H., & García‐García, A. (2022) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-022-02276-6 · Cited by 8 · see citing works
“Notably, it has been reported that although long-life treatment may conduce to developing a diabetes-like condition (Blagosklonny 2011), it is reversible and does not lead to complications (Blagosklonny 2019).”
BackgroundCurrent Dietary Lipids Recommendations: Pros and Cons
Giraudo, S., Montero, J. C., Kaufmann, P., & Grossman, B. (2016) · Journal of Nutrition and Health Sciences · doi:10.15744/2393-9060.3.406 · Cited by 3 · see citing works
Pharmacokinetics of long-term low-dose oral rapamycin in four healthy middle-aged companion dogsPreprint
Evans, J. B., Morrison, A. J., Javors, M. A., Lopez‐Cruzan, M., Promislow, D., Kaeberlein, M. R., & Creevy, K. E. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.01.20.427425 · Cited by 3 · see citing works
Chaudhary, J. K., & Rath, P. C. (2020) · Springer eBooks · doi:10.1007/978-981-32-9005-1_12 · Cited by 2 · see citing works
ANALISI PROTEOMICA DEL MUSCOLO CARDIACO DI RATTO IN CORSO D'INVECCHIAMENTO
Leone, R. (2014) · Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) · doi:10.13130/leone-roberta_phd2014-02-04
Chronic mTOR Inhibition by Rapamycin and Diabetes
Yan, L., & Cai, Z. (2016) · Elsevier eBooks · doi:10.1016/b978-0-12-802733-2.00009-8
Faculty Opinions recommendation of The hallmarks of aging.
Hickson, I. D., & Mankouri, H. W. (2013) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.718061760.793481794
- Authors
- Blagosklonny, M. V.
- Affiliations
- Roswell Park Comprehensive Cancer Center (US)
- Corresponding author
- Blagosklonny, Mikhail V
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2011-12-15
- Volume
- 10
- Issue
- 24
- Pages
- 4217-4224
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- OpenAlex
- W1981104548
- Cited by
- 59
- References
- 0
- Citations by year
- 2025: 1 · 2022: 3 · 2021: 2 · 2020: 2 · 2019: 4 · 2018: 4 · 2017: 2 · 2016: 5 · 2015: 5 · 2014: 10 · 2013: 9 · 2012: 11
- FWCI
- 3.64
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Physiology › Dietary Effects on Health
- Keywords
- rapamycin, impaired glucose tolerance, type 2 diabetes, caloric restriction, insulin resistance, hepatic insulin resistance, gluconeogenesis, healthspan, diabetes complications
- MeSH terms
- Diabetes Mellitus, Type 2, Humans, Insulin Resistance, Models, Biological, Glucose Intolerance, Ribosomal Protein S6 Kinases, Sirolimus, Caloric Restriction, Diabetes Complications, Insulin-Secreting Cells, TOR Serine-Threonine Kinases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review