C-Peptide and leptin system in dichorionic, small and appropriate for gestational age twins-possible link to metabolic programming?

Tytuł:: C-Peptide and leptin system in dichorionic, small and appropriate for gestational age twins-possible link to metabolic programming?
Autorzy:: Lewandowski KC; Department of Endocrinology and Metabolic Diseases, Polish Mothers' Memorial Hospital-Research Institute, Lodz, Poland.; Medical University of Lodz, Department of Endocrinology and Metabolic Diseases, Lodz, Poland.
Biesiada L; Department of Obstetrics and Gynecology, Polish Mother's Memorial Hospital-Research Institute, Lodz, Poland.
Grzesiak M; Department of Perinatology, Obstetrics and Gynecology, Polish Mother's Memorial Hospital-Research Institute, Lodz, Poland.
Sakowicz A; Medical University of Lodz, Department of Medical Biotechnology, Lodz, Poland. .
Źródło:: Nutrition & diabetes [Nutr Diabetes] 2020 Aug 10; Vol. 10 (1), pp. 29. Date of Electronic Publication: 2020 Aug 10.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Original Publication: Houndmills, Basingstoke : Nature Pub. Group, 2010-
MeSH Terms:: Twins*
Blood Glucose/*analysis
C-Peptide/*blood
Infant, Small for Gestational Age/*blood
Receptors, Leptin/*blood
Body Weight ; Diabetes Mellitus, Type 2/epidemiology ; Female ; Fetal Growth Retardation/blood ; Fetal Growth Retardation/epidemiology ; Fetus/metabolism ; Gestational Age ; Glucose Intolerance/epidemiology ; Humans ; Infant, Newborn ; Insulin/blood ; Insulin Resistance ; Leptin/blood ; Male ; Placenta/metabolism ; Pregnancy
References:: Barker, D. J. P. & Osmond, C. Infant mortality, childhood nutrition, and ischaemic heart disease in England and Wales. Lancet 327, 1077–1081 (1986). (PMID: 10.1016/S0140-6736(86)91340-1)
Barker, D. J. P., Osmond, C., Winter, P. D. & Margetts, B. Weight in infancy and death from ischaemic heart disease. Vol. 2, In Lancet 984–985 (London, England, 1989).
Barker, D. J. P. The origins of the developmental origins theory. J. Intern. Med. 261, 412–417 (2007). (PMID: 10.1111/j.1365-2796.2007.01809.x)
Hales, C. N. & Barker, D. J. The thrifty phenotype hypothesis. Br. Med. Bull. 60, 5–20 (2001). (PMID: 10.1093/bmb/60.1.5)
Faraci, M. et al. Fetal growth restriction: current perspectives. J. Prenat. Med. 5, 31–33 (2011). (PMID: 224390733279162)
Hales, C. N. et al. Fetal and infant growth and impaired glucose tolerance at age 64. BMJ 303, 1019–1022 (1991). (PMID: 10.1136/bmj.303.6809.1019)
Poulsen, P., Vaag, A. A., Kyvik, K. O., Jensen, D. M. & Beck-Nielsen, H. Low birth weight is associated with non-insulin-dependent diabetes mellitus in discordant monozygotic and dizygotic twins. Ugeskr Laeger 160, 2382–2387 (1998). (PMID: 9571811)
Saisho, Y. Postprandial C-peptide to glucose ratio as a marker of beta cell function: implication for the management of type 2 diabetes. Int. J. Mol. Sci. 17, 744 (2016). (PMID: 10.3390/ijms17050744)
O'Rahilly, S., Burnett, M. A., Smith, R. F., Darley, J. H. & Turner, R. C. Haemolysis affects insulin but not C-peptide immunoassay. Diabetologia 30, 394–396 (1987). (PMID: 10.1007/BF00292540)
Lewandowski, K. et al. Free leptin, bound leptin, and soluble leptin receptor in normal and diabetic pregnancies. J. Clin. Endocrinol. Metab. 84, 300–306 (1999). (PMID: 10.1210/jcem.84.1.5401)
Lewandowski, K. et al. Effects of insulin and glucocorticoids on the leptin system are mediated through free leptin. Clin. Endocrinol. 54, 533–539 (2001). (PMID: 10.1046/j.1365-2265.2001.01243.x)
Hassink, S. G. et al. Placental leptin: an important new growth factor in intrauterine and neonatal development? Pediatrics 100, E1 (1997). (PMID: 10.1542/peds.100.1.e1)
Gruzdeva, O., Borodkina, D., Uchasova, E., Dyleva, Y. & Barbarash, O. Leptin resistance: underlying mechanisms and diagnosis. Diabetes Metab. Syndr. Obes. 12, 191–198 (2019). (PMID: 10.2147/DMSO.S182406)
Kelesidis, T., Kelesidis, I., Chou, S. & Mantzoros, C. S. Narrative review: the role of leptin in human physiology: emerging clinical applications. Ann. Intern. Med. 152, 93–100 (2010). (PMID: 10.7326/0003-4819-152-2-201001190-00008)
Perez-Perez, A. et al. MAPK and PI3K activities are required for leptin stimulation of protein synthesis in human trophoblastic cells. Biochem. Biophys. Res. Commun. 396, 956–960 (2010). (PMID: 10.1016/j.bbrc.2010.05.031)
Maltepe, E., Bakardjiev, A. I. & Fisher, S. J. The placenta: transcriptional, epigenetic, and physiological integration during development. J. Clin. Invest. 120, 1016–1025 (2010). (PMID: 10.1172/JCI41211)
Schubring, C., Kiess, W., Englaro, P., Rascher, W. & Blum, W. Leptin concentrations in amniotic fluid, venous and arterial cord blood and maternal serum: high leptin synthesis in the fetus and inverse correlation with placental weight. Eur. J. Pediatr. 155, 830 (1996). (PMID: 10.1007/BF02002918)
Linnemann, K., Malek, A., Schneider, H. & Fusch, C. Physiological and pathological regulation of feto/placento/maternal leptin expression. Biochem. Soc. Trans. 29, 86–90 (2001). (PMID: 10.1042/bst0290086)
Yuen, B. S. et al. Leptin alters the structural and functional characteristics of adipose tissue before birth. FASEB J. 17, 1102–1104 (2003). (PMID: 10.1096/fj.02-0756fje)
Yuen, B. S. J. et al. Effects of leptin on fetal plasma adrenocorticotropic hormone and cortisol concentrations and the timing of parturition in the Sheep1. Biol. Reprod. 70, 1650–1657 (2004). (PMID: 10.1095/biolreprod.103.025254)
U.S. Department of Health and Human Services Food and Drug Administration. Guidance for Industry Bioanalytical Method Validation Guidance for Industry Bioanalytical Method Validation. In Biopharmaceutics (2018).
Matthews, D. R. et al. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 28, 412–419 (1985). (PMID: 38998253899825)
Takaya, J., Tanabe, Y., Kuroyanagi, Y. & Kaneko, K. Relationship between asymmetric dimethylarginine in umbilical cord plasma and birth weight follows a U-shaped curve. Endocr. J. 64, 431–436 (2017). (PMID: 10.1507/endocrj.EJ16-0378)
Milenkovic, S. et al. Lipids and adipokines in cord blood and at 72 h in discordant dichorionic twins. Fetal Pediatr. Pathol. 36, 106–122 (2017). (PMID: 10.1080/15513815.2016.1242675)
Verhaeghe, J. et al. C-peptide, insulin-like growth factors I and II, and insulin-like growth factor binding protein-1 in cord serum of twins: genetic versus environmental regulation. Am. J. Obstet. Gynecol. 175, 1180–1188 (1996). (PMID: 10.1016/S0002-9378(96)70025-X)
Geremia, C. & Cianfarani, S. Insulin sensitivity in children born small for gestational age (SGA). Rev. Diabet. Stud. 1, 58–65 (2004). (PMID: 10.1900/RDS.2004.1.58)
Hrebicek, J., Janout, V., Malincikova, J., Horakova, D. & Cizek, L. Detection of insulin resistance by simple quantitative insulin sensitivity check index QUICKI for epidemiological assessment and prevention. J. Clin. Endocrinol. Metab. 87, 144–147 (2002). (PMID: 10.1210/jc.87.1.144)
Lewi, L., Deprest, J. & Hecher, K. The vascular anastomoses in monochorionic twin pregnancies. YMOB 208, 19–30 (2013).
Smfm, M. M. & Simpson, L. L. SMFM clinical guideline twin-twin transfusion syndrome. YMOB 208, 3–18 (2013).
Rinaudo, P. & Wang, E. Fetal programming and metabolic syndrome. Annu. Rev. Physiol. 74, 107–130 (2012). (PMID: 10.1146/annurev-physiol-020911-153245)
Srinivasan, M. & Patel, M. S. Metabolic programming in the immediate postnatal period. Trends Endocrinol. Metab. 19, 146–152 (2008). (PMID: 10.1016/j.tem.2007.12.001)
Takaya, J., Yamato, F., Higashino, H. & Kaneko, K. Intracellular magnesium and adipokines in umbilical cord. Pediatr. Res. 62, 700–703 (2007). (PMID: 10.1203/PDR.0b013e318157d219)
Tzschoppe, A. et al. Intrauterine growth restriction (IUGR) is associated with increased leptin synthesis and binding capability in neonates. Clin. Endocrinol. 74, 459–466 (2011). (PMID: 10.1111/j.1365-2265.2010.03943.x)
Takahashi, N., Waelput, W. & Guisez, Y. Leptin is an endogenous protective protein against the toxicity exerted by tumor necrosis factor. J. Exp. Med. 189, 207–212 (1999). (PMID: 10.1084/jem.189.1.207-a)
Pedroso, A. P. et al. Intrauterine growth restriction programs the hypothalamus of adult male rats: integrated analysis of proteomic and metabolomic data. J. Proteome Res. 16, 1515–1525 (2017). (PMID: 10.1021/acs.jproteome.6b00923)
Perez-Perez, A. et al. Leptin reduces apoptosis triggered by high temperature in human placental villous explants: The role of the p53 pathway. Placenta 42, 106–113 (2016). (PMID: 10.1016/j.placenta.2016.03.009)
Gonzalez, R. R. et al. Leptin signaling promotes the growth of mammary tumors and increases the expression of vascular endothelial growth factor (VEGF) and its receptor type two (VEGF-R2). J. Biol. Chem. 281, 26320–26328 (2006). (PMID: 10.1074/jbc.M601991200)
Klaffenbach, D. et al. Upregulation of leptin-receptor in placental cells by hypoxia. Regul. Pept. 167, 156–162 (2011). (PMID: 10.1016/j.regpep.2010.12.007)
Lewandowski, K. C., Plusajska, J., Horzelski, W., Bieniek, E. & Lewinski, A. Limitations of insulin resistance assessment in polycystic ovary syndrome. Endocr. Connect 7, 403–412 (2018). (PMID: 10.1530/EC-18-0021)
Substance Nomenclature:: 0 (Blood Glucose)
0 (C-Peptide)
0 (Insulin)
0 (Leptin)
0 (Receptors, Leptin)
Entry Date(s):: Date Created: 20200812 Date Completed: 20210330 Latest Revision: 20210330
Update Code:: 20240105
PubMed Central ID:: PMC7417567
DOI:: 10.1038/s41387-020-00131-2
PMID:: 32778645
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Children born small for gestational age (SGA) are at increased risk of future glucose intolerance and type 2 diabetes, possibly after due intrauterine metabolic programming. Soluble leptin receptor (SLR) limits leptin access to signal-transducing membrane receptors. The present study examines whether SGA and appropriate for gestational age (AGA) twins differ with regard to their C-peptide, glucose and leptin systems. The markers C-peptide, glucose, fetal leptin, and SLR in cord blood were assessed in children from dichorionic twin pregnancies at delivery. In 32 cases, weight differed by >15% between twins: one demonstrated Intrauterine Growth Retardation (IUGR) (<10th percentile-SGA), while the other did not (AGA I ). The other 67 pairs presented appropriate weight for gestational age (AGA II ). Placental leptin and placental leptin receptor content were also assessed. Despite the same concentrations of glucose, the SGA twins maintained a higher level of C-peptide [44.48 pmol/l vs. 20.91 pmol/l, p < 0.05] than the AGA I co-twins, higher HOMA index, calculated as [C-peptide] x [Glucose] (p = 0.045), in cord blood, and a higher level of SLR [SGA vs AGA I -mean: 28.63 ng/ml vs. 19.91 ng/ml, p < 0.01], without any differences in total leptin (p = 0.37). However, SGA placentas demonstrated higher leptin level [130.1 pg/100 g total protein vs 83.8 pg/100 g total protein, p = 0.03], without differences in placental leptin receptor (p = 0.66). SGA/IUGR twins demonstrate relative insulin resistance accompanied by decreased fetal and increased placental leptin signaling. We speculate that relative insulin resistance and changes in the leptin system might be the first evidence of processes promoting deleterious metabolic programming for post-natal life.

Erratum in: Nutr Diabetes. 2020 Aug 24;10(1):32. (PMID: 32839426)

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