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Heritability of Insulin Secretion, Peripheral and Hepatic Insulin Action, and Intracellular Glucose Partitioning in Young and Old Danish Twins
Open accessAbstract
The etiology of type 2 diabetes is multifactorial, including genetic as well as pre- and postnatal factors that influence several different defects of glucose homeostasis, primarily in muscle, β-cells, and liver. In the present twin study, we report heritability estimates (h2) for measures of insulin secretion, insulin resistance, hepatic glucose production (HGP), and intracellular glucose partitioning using gold standard methods (euglycemic-hyperinsulinemic clamp technique, tritiated glucose infusion, indirect calorimetry, and intravenous glucose tolerance testing) among 110 younger (22–31 years of age) and 86 older (57–66 years of age) twins. To obtain a valid estimate of β-cell function, insulin secretion was adjusted for the individual degree of insulin action (disposition index). In both age-groups there was a major genetic component in the etiology of insulin secretion that was statistically significantly higher among older twins (young h2 = 0.75 [0.55–0.86] and old h2 = 0.84 [0.69–0.92], P < 0.05). The heritability estimates for peripheral insulin sensitivity (young h2 = 0.53 [0.28–0.71] and old h2 = 0.55 [0.20–0.76]) and nonoxidative glucose metabolism (young h2 = 0.50 [0.32–0.64] and old h2 = 0.48 [0.04–0.72]) were similar in younger and older twins, supporting the notion of both genetic and environmental etiological factors in the control of insulin action and nonoxidative glucose metabolism. The results suggested that HGP was predominantly controlled by nongenetic factors in both young and old twins. In conclusion, we provide further evidence for a role of genes in controlling insulin secretion, insulin action, and nonoxidative glucose metabolism. The relative contribution of genes versus environment on in vivo insulin secretion exhibited an age dependency with a slightly greater relative impact of genes among older as compared with younger twins.
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“Similarly, a genetic predisposition to defective insulin secretion when combined with insulin resistance can raise plasma glucose to abnormal levels.57”
From Diagnosis and Management of the Metabolic Syndrome: An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement (2005) · cites this paper as [57]
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BackgroundSelf-citationDiagnosis and management of the metabolic syndrome
Grundy, S. M., Cleeman, J. I., Daniels, S. R., Donato, K. A., Eckel, R. H., Franklin, B. A., Gordon, D. J., Krauss, R. M., Savage, P. J., Smith, S. C., et al. (2005) · Current Opinion in Cardiology · doi:10.1097/01.hco.0000200416.65370.a0 · Cited by 437
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“In contrast to findings from twin studies [28, 31] and one family study [24] the OGTT-based measures of insulin Diabetologia (2011) 54:2811–2819 2817”
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Self-citationMetabolic syndrome and cardiovascular risk
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“[28] Although the metabolic syndrome unequivocally predisposes to type 2 diabetes mellitus, [29] many investigators of cardiovascular diseases consider this syndrome a multidimensional risk factor for ASCVD.”
BackgroundAge influences DNA methylation and gene expression of COX7A1 in human skeletal muscle.
Rönn, T., Poulsen, P., Hansson, O., Holmkvist, J., Almgren, P., Nilsson, P., Tuomi, T., Isomaa, B., Groop, L., Vaag, A., et al. (2008) · Diabetologia · doi:10.1007/s00125-008-1018-8 · Cited by 175
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MethodSelf-citationInsulin Resistance in Children
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“Acute serum insulin response 0–10 min, hepatic glucose production, and glucose disposal rate are calculated as described elsewhere (18) and in the online appendix.”
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“than MZT twins (mean age [range]: 49 [22-76] and 29 [18-47] years, respectively, Table 1).”
BackgroundPathomechanisms of Type 2 Diabetes Genes
Staiger, H., Machicao, F. E., Fritsche, A., & Häring, H.-U. (2009) · Endocrine Reviews · doi:10.1210/er.2009-0017 · Cited by 141
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“6) (Edwards et al., 1997; Hsueh et al., 2000; Freeman et al., 2002;Mills et al., 2004; Poulsen et al., 2005; Lehtovirta et al., 2005; Bayoumi et al., 2007).”
Orchestration of Glucose Homeostasis
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“Poulsen and colleagues used state-of-the-art methodology to measure a variety of metabolic parameters in monozygotic and dizygotic Danish twins (50).”
BackgroundMethodDing, M., Chavarro, J. E., Olsen, S. F., Lin, Y., Ley, S. H., Bao, W., Rawal, S., Grunnet, L. G., Thuesen, A. C. B., Mills, J. L., et al. (2018) · Diabetologia · doi:10.1007/s00125-018-4637-8 · Cited by 106
“More than 53% of peripheral insulin sensitivity and 75% of the variation in insulin secretion can be explained by genetic components [20, 21].”
Self-citationShaat, N., Lernmark, Å., Karlsson, E., Ivarsson, S. A., Parikh, H. M., Berntorp, K. E., & Groop, L. (2007) · Diabetologia · doi:10.1007/s00125-007-0623-2 · Cited by 108
“Both insulin deficiency and insulin resistance are considered to be heritable with heritability estimates for insulin secretion of 0.75–0.84 and for insulin sensitivity of 0.53–0.55 [ 4 ].”
BackgroundInfluentialCTSH regulates β-cell function and disease progression in newly diagnosed type 1 diabetes patients
Fløyel, T., Brorsson, C., Nielsen, L. B., Miani, M., Bang-Berthelsen, C. H., Friedrichsen, M., Overgaard, A. J., Berchtold, L. A., Wiberg, A., Poulsen, P., et al. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1402571111 · Cited by 104
“young (22–31 y) and 43 old (57–66 y) monozygotic and same sex dizygotic twin pairs without known diabetes (39); however, in this study, we focused on the young twins, because they are most likely more compatible with the T1D”
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Self-citationBoesgaard, T. W., Grarup, N., Jørgensen, T., Borch‐Johnsen, K., Hansen, T. F., & Pedersen, O. B. (2010) · Diabetologia · doi:10.1007/s00125-010-1753-5 · Cited by 99
“These numbers should be interpreted in relation to heritability estimates of 30% to 40% and 60% to 80% for fasting glucose and first-phase insulin release, respectively [32], indicating that 15% to 20% and 5% to 10%, respectively, of the genetic contribution to these traits has been accounted for.”
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“Furthermore, evidence indicates that -cell function may be more highly determined by heritable factors compared with other known pathogenic traits involved in type 2 diabetes (17).”
BackgroundInsulin signaling regulating genes: effect on T2DM and cardiovascular risk
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“The heritability of insulin secretion is higher than that of insulin resistance (3).”
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“In studies of twins, 50% of the variance in insulin sensitivity and secretionwas attributed to genetic factors [31].”
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“We have previously found an influence of zygosity on insulin-stimulated glucose uptake, with elderly MZ twins being more insulin resistant compared with DZ twins (9,17).”
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Impact ofTCF7L2rs7903146 on Insulin Secretion and Action in Young and Elderly Danish Twins
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Self-citationBork‐Jensen, J., Schéele, C., Christophersen, D. V., Nilsson, E., Friedrichsen, M. H., Fernandez‐Twinn, D. S., Grunnet, L. G., Litman, T., Holmstrøm, K., Vind, B. F., et al. (2014) · Diabetologia · doi:10.1007/s00125-014-3434-2 · Cited by 68
“The non-diabetic twin population was a subgroup of 164 MZ and same-sex dizygotic (DZ) twins (the number of individuals with available tissue material) from a previously described population [7] of 196 young and old twins (aged 25– 32 and 58–66 years).”
Self-citationRetinol-Binding Protein 4 in Twins
Ribel‐Madsen, R., Friedrichsen, M. H., Vaag, A. A., & Poulsen, P. (2008) · Diabetes · doi:10.2337/db08-1019 · Cited by 62
“-Cell function was estimated from an intravenous glucose tolerance test by calculation of the first-phase disposition index (Di1) (20).”
MethodInfluentialSelf-citationPhysiologic Characterization of Type 2 Diabetes–Related Loci
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“Both basal and insulin-stimulated glucose uptake are also in part genetically determined, with heritability estimates ranging from 40% to 60% [10, 12, 13].”
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The Association Between Low Birth Weight and Type 2 Diabetes
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Twins in metabolic and diabetes research: what do they tell us?
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Self-citationThe Architecture of Risk for Type 2 Diabetes: Understanding Asia in the Context of Global Findings
Abdullah, N., Attia, J., Oldmeadow, C. J., Scott, R. J., & Holliday, E. G. (2014) · International Journal of Endocrinology · doi:10.1155/2014/593982 · Cited by 47
“Twin studies also demonstrate a substantial genetic component for quantitative phenotypes related to glucose homeostasis, with heritability estimates of 75–85% for in vivo insulin secretion, ∼50% for peripheral insulin sensitivity, and ∼50% for glucose metabolism [82].”
BackgroundBanasik, K., Ribel‐Madsen, R., Gjesing, A. P., Thørner, L. W., Andersson, Å., Poulsen, P., Borglykke, A., Witte, D. R., Pedersen, O. B., Hansen, T. F., et al. (2010) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2010-0881 · Cited by 47
Self-citationA genome-wide association study of gestational diabetes mellitus in Chinese women
Wu, N., Zhao, D., Ma, W., Lang, J., Liu, S., Fu, Y., Wang, X., Wang, Z., & Li, Q. (2019) · The Journal of Maternal-Fetal & Neonatal Medicine · doi:10.1080/14767058.2019.1640205 · Cited by 41
Heritability and genetic correlations of insulin sensitivity measured by the euglycaemic clamp
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The ENPP1 Q121 Variant Predicts Major Cardiovascular Events in High-Risk Individuals
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ADAMTS9 Regulates Skeletal Muscle Insulin Sensitivity Through Extracellular Matrix Alterations
Graae, A.-S., Grarup, N., Ribel‐Madsen, R., Lystbæk, S. H., Boesgaard, T. W., Staiger, H., Fritsche, A., Wellner, N., Sulek, K., Kjølby, M., et al. (2019) · Diabetes · doi:10.2337/db18-0418 · Cited by 39
“Study Populations Study participants from six different study populations were included: Uppsala Longitudinal Study of Adult Men (ULSAM) (18), Danish young healthy individuals (19), Danish nondiabetic twin cohort (20), EUGENE2 (European Network on Functional Genomics of Type 2 Diabetes) (5), Danish family study (21),…”
BackgroundSelf-citationGoodarzi, M. O., Langefeld, C. D., Xiang, A. H., Chen, Y. I., Guo, X., Hanley, A. J., Raffel, L. J., KANDEEL, F. R., Nadler, J. L., Buchanan, T. A., et al. (2013) · Obesity · doi:10.1002/oby.20639 · Cited by 39
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“The clinical examinations of the YOND cohort (n = 192) and the Inter99 subset (n = 63) have previously been described in detail [20,21,23].”
MethodSelf-citationRönn, T., Poulsen, P., Tuomi, T., Isomaa, B., Groop, L., Vaag, A., & Ling, C. (2009) · PLoS ONE · doi:10.1371/journal.pone.0004793 · Cited by 36
“The subjects underwent a 2-hour hyperinsulinemic euglycemic clamp (40 mU m(22) min(21)) combined with indirect calorimetry during the basal and insulin-stimulated steady state periods as previously described [14].”
MethodSelf-citationMolecular correlates for maximal oxygen uptake and type 1 fibers
Parikh, H., Nilsson, E., Ling, C., Poulsen, P., Almgren, P., Nittby, H., Eriksson, K.-F., Vaag, A., & Groop, L. C. (2008) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.90255.2008 · Cited by 36
“Details of this study have been described previously (16, 27).”
MethodSelf-citationGenetic and metabolic effects on skeletal muscle AMPK in young and older twins
Mortensen, B., Poulsen, P., Wegner, L., Stender-Petersen, K. L., Ribel-Madsen, R., Friedrichsen, M., Birk, J. B., Vaag, A., & Wojtaszewski, J. F. P. (2009) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00058.2009 · Cited by 36
“It is well known that genetic factors predispose to the development of type 2 diabetes (32, 34).”
BackgroundSelf-citationGene–Nutrient Interactions in the Metabolic Syndrome
Phillips, C. M., Tierney, A. C., & Roche, H. M. (2008) · Lifestyle Genomics · doi:10.1159/000112461 · Cited by 36
“In contrast, the heritability estimates for hyperinsulinaemia, hypertension and hypertriacylglycerolaemia are low, indicating a more important environmental influence on these components of the MetS. More recently, results from a comprehensive study examining young and elderly monozygotic and dizygotic twins provided…”
ResultGenetic influences on the insulin response of the beta cell to different secretagogues
Simonis-Bik, A. M. C., Eekhoff, E. M. W., de Moor, M. H. M., Kramer, M. H. H., Boomsma, D. I., Heine, R. J., Dekker, J. M., Maassen, J. A., Hart, L. M. ‘., Diamant, M., et al. (2009) · Diabetologia · doi:10.1007/s00125-009-1532-3 · Cited by 34
“Two twin studies, for instance, showed a significant genetic contribution to insulin sensitivity, assessed by euglycaemic–hyperinsulinaemic clamp with heritability estimates of 37% and 55% [11, 12].”
BackgroundResultBloomfield, F. H., Oliver, M. H., & Harding, J. E. (2006) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00210.2006 · Cited by 33
“In some cases, the most affected subjects have been excluded, such as the exclusion of diabetic subjects in studies of glucose tolerance (50, 51).”
BackgroundGenetic and Nongenetic Regulation of CAPN10 mRNA Expression in Skeletal Muscle
Carlsson, E., Poulsen, P., Storgaard, H., Almgren, P., Ling, C., Jensen, C. B., Madsbad, S., Groop, L., Vaag, A. A., & Ridderstråle, M. (2005) · Diabetes · doi:10.2337/diabetes.54.10.3015 · Cited by 33
Self-citationFriedrichsen, M. H., Poulsen, P., Wojtaszewski, J. F. P., Hansen, P. R., Vaag, A. A., & Rasmussen, H. B. (2013) · PLoS ONE · doi:10.1371/journal.pone.0056861 · Cited by 33
“Although it is known that insulin sensitivity is under strong genetic control [44,45], very few genetic variations affecting insulin sensitivity in the liver or skeletal muscle have been identified so far.”
BackgroundSelf-citationMcElfish, P. A., Narcisse, M., Long, C. R., Ayers, B. L., Hawley, N. L., Aitaoto, N., Riklon, S., Su, L. J., Ima, S., Wilmoth, R. O., et al. (2017) · Journal of Community Genetics · doi:10.1007/s12687-017-0313-9 · Cited by 30
“…is typically understood to result from interaction between environmental factors and a strong hereditary component (estimates of heritability range from 20 to 80% depending on the population studied) (Alberti et al. 2007; Ali 2013; Kaprio et al. 1992; Meigs et al. 2000; Poulsen et al. 2005).”
BackgroundRose, C. S., Grarup, N., Krarup, N. T., Poulsen, P., Wegner, L., Nielsen, T., Banasik, K., Færch, K., Andersen, G., Albrechtsen, A., et al. (2009) · Diabetologia · doi:10.1007/s00125-009-1463-z · Cited by 30
“Additionally, rs560887 was examined in a sample of 53 elderly and 106 young twins with normal glucose tolerance subjected to a 2 h hyperinsulinaemic–euglycaemic clamp (40 mU m min) with measures of hepatic glucose production during the fasting state and upon insulin infusion [13].”
MethodSelf-citationRasouli, N., Hale, T. C., Kahn, S. E., Spencer, H. J., & Elbein, S. C. (2005) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2005-0048 · Cited by 29
Wang, X., Li, W., Ma, L., Gao, J., Liu, J., Ping, F., & Nie, M. (2015) · Acta Diabetologica · doi:10.1007/s00592-015-0768-2 · Cited by 28
“by a combination of genetic factors and environmental exposure, with genetic components being the major determinant of disease [19]; however, the genetic mechanism”
BackgroundFirneisz, G., Rosta, K., Al‐Aissa, Z., Hadarits, O., Harreiter, J., Nádasdi, Á., Bancher‐Todesca, D., Németh, L., Igaz, P., Rigó, J. J., et al. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19123734 · Cited by 30
Poulsen, P., Wojtaszewski, J. F. P., Petersen, I., Christensen, K., Richter, E. A., Beck‐Nielsen, H., & Vaag, A. A. (2005) · Diabetes · doi:10.2337/diabetes.54.5.1289 · Cited by 28
“Subjects were identified through the Danish Twin Register (19), as previously described.”
BackgroundMethodResultInfluentialSelf-citationPhysical inactivity affects skeletal muscle insulin signaling in a birth weight-dependent manner
Mortensen, B., Friedrichsen, M. H., Andersen, N. R., Alibegovic, A. C., Højbjerre, L., Sonne, M. P., Stallknecht, B. M., Dela, F., Wojtaszewski, J. F. P., & Vaag, A. A. (2013) · Journal of Diabetes and its Complications · doi:10.1016/j.jdiacomp.2013.09.002 · Cited by 27
Self-citationGrenier–Larouche, T., Carreau, A., & Carpentier, A. C. (2017) · Canadian Journal of Diabetes · doi:10.1016/j.jcjd.2016.10.013 · Cited by 26
Wang, X., Li, W., Ma, L., Ping, F., Liu, J., Wu, X., Mao, J., Wang, X., & Nie, M. (2017) · Acta Diabetologica · doi:10.1007/s00592-017-0969-y · Cited by 25
Storgaard, H., Poulsen, P., Ling, C., Groop, L., & Vaag, A. A. (2007) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2006-1812 · Cited by 25
Self-citationTantari, G., Bassi, M., Pistorio, A., Minuto, N., Napoli, F., Piccolo, G., Valle, A. L., Spacco, G., Cervello, C., d’Annunzio, G., et al. (2024) · Frontiers in Endocrinology · doi:10.3389/fendo.2024.1439901 · Cited by 24
Association between dietary fat intake and insulin resistance in Chinese child twins
Huang, T., Beaty, T. H., Li, J., Liu, H., Zhao, W., & Wang, Y. (2017) · British Journal Of Nutrition · doi:10.1017/s0007114516004542 · Cited by 24
“Our results are consistent with previous evidences showing estimated heritability for peripheral IS (h(2) 0·53) and non-oxidative glucose metabolism (h(2) 0·50) in young people, supporting the notion that there are both genetic and environmental aetiological factors controlling insulin action and non-oxidative glucose…”
ResultHingst, J. R., Onslev, J., Holm, S. K., Kjøbsted, R., Frøsig, C., Kido, K., Steenberg, D. E., Larsen, M. R., Kristensen, J. M., Carl, C. S., et al. (2022) · Diabetes · doi:10.2337/db22-0015 · Cited by 25
Transcription factor 7-like 2 gene polymorphisms and gestational diabetes mellitus
Klein, K., Haslinger, P., Bancher‐Todesca, D., Leipold, H., Knöfler, M., Handisurya, A., Kautzky‐Willer, A., & Worda, C. (2012) · The Journal of Maternal-Fetal & Neonatal Medicine · doi:10.3109/14767058.2012.663831 · Cited by 24
van Hoek, M., van Herpt, T. T. W., Dehghan, A., Hofman, A., Lieverse, A. G., van Duijn, C. M., Witteman, J. C. M., & Sijbrands, E. J. G. (2011) · Diabetologia · doi:10.1007/s00125-011-2092-x · Cited by 24
“Defective insulin secretion has higher heritability estimates than insulin resistance in family and twin studies [8–10], and the concordance rate for type 2 diabetes in lean twins is higher than that in obese twins [11].”
BackgroundGrunnet, L. G., Poulsen, P., Pedersen, B. K., Mandrup-Poulsen, T. R., & Vaag, A. A. (2005) · Diabetologia · doi:10.1007/s00125-005-0080-8 · Cited by 24
“Furthermore, we applied biometric modelling to estimate the relative impact of additive and dominant genetic effects, as well as the relative impact of unique and shared environmental effects [19, 22].”
BackgroundMethodResultInfluentialSelf-citationThe Impact of Genetic Variation in theG6PC2Gene on Insulin Secretion Depends on Glycemia
Heni, M., Ketterer, C., Hart, L. M. ‘., Ranta, F., van Haeften, T. W., Eekhoff, E. M. W., Dekker, J. M., Boomsma, D. I., Nijpels, G., Kramer, M. H. H., et al. (2010) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2010-0860 · Cited by 23
Olsson, A. H., Rönn, T., Elgzyri, T., Hansson, O., Eriksson, K., Groop, L., Vaag, A. A., Poulsen, P., & Ling, C. (2011) · Molecular Genetics and Metabolism · doi:10.1016/j.ymgme.2011.03.017 · Cited by 22
Self-citationThe effect of physical exercise and caloric restriction on the components of metabolic syndrome
Torres‐Leal, F. L., de Capitani, M. D., & Tirapegui, J. (2009) · Brazilian Journal of Pharmaceutical Sciences · doi:10.1590/s1984-82502009000300003 · Cited by 24
“Although hyperinsulinemia and insulin resistance are the main features of MS, the etiology of MS is still not clear, with some researchers suggesting the involvement of genetic and environmental factors (ATPIII, 2001; Martin et al., 2003; Poulsen et al., 2005).”
BackgroundGranhall, C., Rosengren, A., Renström, E., & Luthman, H. (2006) · Diabetes · doi:10.2337/db06-0796 · Cited by 21
Insulin Promoter Factor 1 variation is associated with type 2 diabetes in African Americans
Karim, M. A., Wang, X., Hale, T. C., & Elbein, S. C. (2005) · BMC Medical Genetics · doi:10.1186/1471-2350-6-37 · Cited by 21
“Impaired β-cell function predicts future diabetes [3], and work from our laboratory [4] and others [5,6] suggest that the ability of the pancreatic β-cell to compensate for prevailing insulin sensitivity (ie, β-cell compensation) is highly heritable.”
Lehtovirta, M., Kaprio, J. A., Groop, L., Trombetta, M., & Bonadonna, R. C. (2005) · Diabetologia · doi:10.1007/s00125-005-1815-2 · Cited by 21
“84 in a population consisting of young and old MZ and DZ twins [34].”
BackgroundFriedrichsen, M. H., Birk, J. B., Richter, E. A., Ribel‐Madsen, R., Pehmøller, C. K., Hansen, B. F., Beck‐Nielsen, H., Hirshman, M. F., Goodyear, L. J., Vaag, A. A., et al. (2013) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00494.2012 · Cited by 22
Self-citationXie, K., Chen, T., Zhang, Y., Wen, J., Cui, X., You, L., Zhu, L., Xu, B., Ji, C., & Guo, X. (2019) · Scientific Reports · doi:10.1038/s41598-019-41605-3 · Cited by 20
Genetic Associations with Diabetes: Meta-Analyses of 10 Candidate Polymorphisms
Tang, L., Wang, L., Liao, Q., Wang, Q., Xu, L., Bu, S., Huang, Y., Zhang, C., Ye, H., Xu, X., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0070301 · Cited by 19
“Besides environmental factors, twin studies have demonstrated a strong heritability for diabetes [4,5] and insulin related phenotypes [6–8].”
BackgroundA common variation of the PTEN gene is associated with peripheral insulin resistance
Grinder-Hansen, L., Ribel‐Madsen, R., Wojtaszewski, J. F. P., Poulsen, P., Grunnet, L. G., & Vaag, A. A. (2016) · Diabetes & Metabolism · doi:10.1016/j.diabet.2016.03.003 · Cited by 19
Self-citationAssessment of age-related changes in heritability and IGF-1 gene effect on circulating IGF-1 levels
Franco, L., Williams, F. M. K., Trofimov, S., Malkin, I., Surdulescu, G. L., Spector, T. D., & Livshits, G. (2014) · AGE · doi:10.1007/s11357-014-9622-7 · Cited by 18
“86)] (Poulsen et al. 2005).”
ResultInfluentialStorgaard, H., Poulsen, P., Ling, C., Groop, L., & Vaag, A. A. (2006) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2005-1172 · Cited by 26
Self-citationFriedrichsen, M. H., Poulsen, P., Richter, E. A., Hansen, B. F., Birk, J. B., Ribel‐Madsen, R., Stender-Petersen, K. L., Nilsson, E., Beck‐Nielsen, H., Vaag, A. A., et al. (2010) · Diabetologia · doi:10.1007/s00125-010-1795-8 · Cited by 16
“Clinical and metabolic characteristics The physiological data from this population have been described in detail [6, 22, 25, 27, 29, 32, 33].”
BackgroundMethodResultInfluentialSelf-citationPrasad, R. B., Kristensen, K. H., Katsarou, A., & Shaat, N. (2021) · BMC Medical Genomics · doi:10.1186/s12920-021-01123-6 · Cited by 18
“Recent evidence suggests that both insulin secretion and resistance are heritable traits [8] and studies have also demonstrated a genetic contribution to defective insulin secretion and resistance in individuals with type 2 diabetes [9, 10].”
BackgroundGene-Physical Activity Interactions and Their Impact on Diabetes
Kilpeläinen, T. O., & Franks, P. W. (2014) · Medicine and sport science/Medicine and sport · doi:10.1159/000357339 · Cited by 16
Overexpression of Gjb4 impairs cell proliferation and insulin secretion in primary islet cells
Gässler, A., Quiclet, C., Kluth, O., Gottmann, P., Schwerbel, K., Helms, A., Stadion, M., Wilhelmi, I., Jonas, W., Ouni, M., et al. (2020) · Molecular Metabolism · doi:10.1016/j.molmet.2020.101042 · Cited by 14
“The role of heritability in T2D has been proven by several twin studies [2,3] and by genome-wide association studies that identified genes and loci that participate in the development of T2D [4].”
ResultFunctional Variant Disrupts Insulin Induction of USF1
Naukkarinen, J., Nilsson, E., Koistinen, H. A., Söderlund, S., Lyssenko, V., Vaag, A. A., Poulsen, P., Groop, L., Taskinen, M., & Peltonen, L. (2009) · Circulation Cardiovascular Genetics · doi:10.1161/circgenetics.108.840421 · Cited by 14
Self-citationGrunnet, L. G., Laurila, E., Hansson, O., Almgren, P., Groop, L., Brøns, C., Poulsen, P., & Vaag, A. A. (2012) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2012-2061 · Cited by 14
Self-citationRegulation of skeletal muscle PPARδ mRNA expression in twins
Nilsson, E., Poulsen, P., Sjögren, M., Ling, C., Ridderstråle, M., Groop, L., & Vaag, A. A. (2007) · The Journal of Physiology · doi:10.1113/jphysiol.2007.140673 · Cited by 14
“Subjects were identified through The Danish Twin Register and selected as previously described (Poulsen et al. 2002, 2005).”
MethodInfluentialSelf-citationNature versus Nurture in Determining Athletic Ability
Brutsaert, T. D., & Parra, E. J. (2009) · Medicine and sport science/Medicine and sport · doi:10.1159/000235694 · Cited by 14
Metadata
- Authors
- Poulsen, P., Levin, K., Petersen, I., Christensen, K., Beck-Nielsen, H., & Vaag, A.
- Affiliations
- Steno Diabetes Center, Gentofte, Denmark
- Odense University Hospital (DK)
- University of Southern Denmark (DK)
- Odense University Hospital, Odense, Denmark
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2005-01-01
- Volume
- 54
- Issue
- 1
- Pages
- 275-283
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2143531355
- Cited by
- 166
- References
- 35
- Citations by year
- 2025: 3 · 2024: 3 · 2023: 1 · 2022: 9 · 2021: 6 · 2020: 4 · 2019: 10 · 2018: 6 · 2017: 7 · 2016: 7 · 2015: 6 · 2014: 10 · 2013: 9 · 2012: 5
- FWCI
- 13.63
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- University of Southern Denmark Research Portal (University of Southern Denmark) (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- heritability, insulin secretion, insulin resistance, hepatic glucose production, beta-cell function, disposition index, nonoxidative glucose metabolism, age differences, genetic versus environmental factors, twins
- MeSH terms
- Insulin Secretion, Adult, Aging, Blood Glucose, Denmark, Female, Glucose, Glycolysis, Humans, Insulin, Liver, Male, Middle Aged, Glucose Clamp Technique
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