Bibliografías temáticas / Insulin resistance

Literatura académica sobre el tema "Insulin resistance"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 6 de julio de 2024

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Artículos de revistas sobre el tema "Insulin resistance"

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Kumar, Sinha Ritesh y Chandra Satish. "Insulin resistance". Asian Pacific Journal of Health Sciences, Supplimentary 2014 (2014): 71–78. http://dx.doi.org/10.21276/apjhs.2014.1.1s.15.

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Sowers, James R. y Edward D. Frohlich. "Insulin and insulin resistance:". Medical Clinics of North America 88, n.º 1 (enero de 2004): 63–82. http://dx.doi.org/10.1016/s0025-7125(03)00128-7.

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Jeffery, Alison. "Insulin resistance". Nursing Standard 17, n.º 32 (23 de abril de 2003): 47–53. http://dx.doi.org/10.7748/ns2003.04.17.32.47.c3381.

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Tomono, Syouichi. "Insulin Resistance :". Kitakanto Medical Journal 62, n.º 1 (2012): 73–74. http://dx.doi.org/10.2974/kmj.62.73.

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Jeffery, Alison. "Insulin resistance". Nursing Standard 17, n.º 32 (23 de abril de 2003): 47–55. http://dx.doi.org/10.7748/ns.17.32.47.s62.

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Park, Kyong Soo. "Insulin Resistance". Journal of the Korean Medical Association 44, n.º 3 (2001): 302. http://dx.doi.org/10.5124/jkma.2001.44.3.302.

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Bell, David S. H. "Insulin resistance". Postgraduate Medicine 93, n.º 7 (15 de mayo de 1993): 99–107. http://dx.doi.org/10.1080/00325481.1993.11701704.

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Carroll, P. B. y R. C. Eastman. "Insulin Resistance". Endocrinologist 1, n.º 2 (abril de 1991): 89–97. http://dx.doi.org/10.1097/00019616-199104000-00005.

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DeFronzo, Ralph A. "Insulin resistance". Current Opinion in Cardiology 5, n.º 5 (octubre de 1990): 592–98. http://dx.doi.org/10.1097/00001573-199010000-00003.

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Whitelaw, D. C. y S. G. Gilbey. "Insulin Resistance". Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 35, n.º 5 (septiembre de 1998): 567–83. http://dx.doi.org/10.1177/000456329803500501.

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Tesis sobre el tema "Insulin resistance"

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Walker, Adrian Bernard. "The effect of insulin on resistance artery function in insulin-resistant states". Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312450.

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Maffeis, Laura <1981&gt. "Correlation between insulin resistance and treatment-resistant acne". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5654/1/maffeis_laura_tesi.pdf.

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Physiologically during puberty and adolescence, when juvenile acne usually appears, the response to a glucose load is increased if compared to the one observed in adult and at pre-pubertal age, while insulin sensitivity is reduced. Insulin is a hormone that acts at different levels along the axis which controls the sex hormones. It increases the release of LH and FSH by pituitary gland, stimulates the synthesis of androgens in the gonads and stimulates the synthesis of androgenic precursors in adrenal glands. Finally, it acts in the liver by inhibiting the synthesis of Sex Hormone Binding Globulin (SHBG). Insulin is also able to act directly on the production of sebum and amplify the effects of Iinsulin Growth Factor-1 in the skin, inhibiting the synthesis of its binding protein (IGF Binding Protein-1). In female subjects with acne and Polycystic Ovary Syndrome (PCOS) insulin resistance is a well known pathogenetic factor, while the relationship between acne and insulin resistance has been poorly investigated in males so far. The purpose of this study is to investigate the correlation between insulin resistance and acne in young males who do not respond to common therapies. Clinical and biochemical parameters of glucose, lipid metabolism, androgens and IGF-1 were evaluated. Insulin resistance was estimated by Homeostasis Model assessment (HOMA-IR) and Oral Glucose Tolerance Test was also performed. We found that subjects with acne had higher Sistolic and Diastolic Blood Pressure, Waist/Hip Ratio, Waist Circumference, 120' OGTT serum insulin and serum IGF-1 and lower HDL-cholesterol than subjects of comparable age and gender without acne. The results thus obtained confirmed what other authors have recently reported about a metabolic imbalance in young males with acne. Furthermore, these results support the hypothesis that insulin resistance might play an important role in the pathogenesis of treatment-resistant acne in males.
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Maffeis, Laura <1981&gt. "Correlation between insulin resistance and treatment-resistant acne". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5654/.

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Physiologically during puberty and adolescence, when juvenile acne usually appears, the response to a glucose load is increased if compared to the one observed in adult and at pre-pubertal age, while insulin sensitivity is reduced. Insulin is a hormone that acts at different levels along the axis which controls the sex hormones. It increases the release of LH and FSH by pituitary gland, stimulates the synthesis of androgens in the gonads and stimulates the synthesis of androgenic precursors in adrenal glands. Finally, it acts in the liver by inhibiting the synthesis of Sex Hormone Binding Globulin (SHBG). Insulin is also able to act directly on the production of sebum and amplify the effects of Iinsulin Growth Factor-1 in the skin, inhibiting the synthesis of its binding protein (IGF Binding Protein-1). In female subjects with acne and Polycystic Ovary Syndrome (PCOS) insulin resistance is a well known pathogenetic factor, while the relationship between acne and insulin resistance has been poorly investigated in males so far. The purpose of this study is to investigate the correlation between insulin resistance and acne in young males who do not respond to common therapies. Clinical and biochemical parameters of glucose, lipid metabolism, androgens and IGF-1 were evaluated. Insulin resistance was estimated by Homeostasis Model assessment (HOMA-IR) and Oral Glucose Tolerance Test was also performed. We found that subjects with acne had higher Sistolic and Diastolic Blood Pressure, Waist/Hip Ratio, Waist Circumference, 120' OGTT serum insulin and serum IGF-1 and lower HDL-cholesterol than subjects of comparable age and gender without acne. The results thus obtained confirmed what other authors have recently reported about a metabolic imbalance in young males with acne. Furthermore, these results support the hypothesis that insulin resistance might play an important role in the pathogenesis of treatment-resistant acne in males.
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Collison, Mary Williamson. "Insulin signalling in insulin resistance and cardiovascular disease syndromes". Thesis, University of Glasgow, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366184.

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Svanfeldt, Monika. "Perioperative nutrition and insulin resistance /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-637-9/.

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Isaksson, Bengt. "Insulin resistance in pancreatic cancer /". Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-493-3/.

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Berends, Lindsey Matara. "Developmental programming of insulin resistance". Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648433.

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Ali, Salmin. "GLUT 4 and Insulin Resistance". Wright State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=wright1409746939.

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Endre, Tomas. "The hypertension-prone man a study on the pathogenesis of hypertension with regard to insulin sensitivity /". Lund : Dept. of Medicine, Lund University, University Hospital MAS, 1997. http://books.google.com/books?id=3UlsAAAAMAAJ.

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Stuart, Charles A., Mary E. A. Howell, Brian M. Cartwright, Melanie P. McCurry, Michelle L. Lee, Michael W. Ramsey y Michael H. Stone. "Insulin Resistance and Muscle Insulin Receptor Substrate-1 Serine Hyperphosphorylation". Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etsu-works/4117.

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Insulin resistance in metabolic syndrome subjects is profound in spite of muscle insulin receptor and insulin-responsive glucose transporter (GLUT4) expression being nearly normal. Insulin receptor tyrosine kinase phosphorylation of insulin receptor substrate-1 (IRS-1) at Tyr896 is a necessary step in insulin stimulation of translocation of GLUT4 to the cell surface. Serine phosphorylation of IRS-1 by some kinases diminishes insulin action in mice. We evaluated the phosphorylation status of muscle IRS-1 in 33 subjects with the metabolic syndrome and seventeen lean controls. Each underwent euglycemic insulin clamps and a thigh muscle biopsy before and after 8 weeks of either strength or endurance training. Muscle IRS-1 phosphorylation at six sites was quantified by immunoblots. Metabolic syndrome muscle IRS-1 had excess phosphorylation at Ser337 and Ser636 but not at Ser307, Ser789, or Ser1101. Ser337 is a target for phosphorylation by glycogen synthase kinase 3 (GSK3) and Ser636 is phosphorylated by c-Jun N-terminal kinase 1 (JNK1). Exercise training without weight loss did not change the IRS-1 serine phosphorylation. These data suggest that baseline hyperphosphorylation of at least two key serines within muscle IRS-1 diminishes the transmission of the insulin signal and thereby decreases the insulin-stimulated translocation of GLUT4. Excess fasting phosphorylation of muscle IRS-1 at Ser636 may be a major cause of the insulin resistance seen in obesity and might prevent improvement in insulin responsiveness when exercise training is not accompanied by weight loss.
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Libros sobre el tema "Insulin resistance"

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Eleazar, Shafrir y Hansen Barbara C, eds. Insulin resistance and insulin resistance syndrome. London: Taylor & Francis, 2002.

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David, Moller, ed. Insulin resistance. Chichester: Wiley, 1993.

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Zeitler, Philip S. y Kristen J. Nadeau, eds. Insulin Resistance. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-25057-7.

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Reaven, Gerald M. y Ami Laws, eds. Insulin Resistance. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1.

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Zeitler, Philip Scott y Kristen J. Nadeau, eds. Insulin Resistance. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-192-5.

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Kumar, Sudhesh y Stephen O'Rahilly, eds. Insulin Resistance. Chichester, UK: John Wiley & Sons, Ltd, 2004. http://dx.doi.org/10.1002/0470011327.

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Krentz, Andrew J., ed. Insulin Resistance. Oxford, UK: Blackwell Science Ltd, 2002. http://dx.doi.org/10.1002/9780470698921.

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Sudhesh, Kumar y O'Rahilly S, eds. Insulin resistance: Insulin action and its disturbances in disease. Chichester, West Sussex, England: J. Wiley, 2005.

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B, Yao E., ed. Insulin resistance: New research. Hauppauge, NY: Nova Science, 2009.

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Fantus, I. George, ed. Insulin Resistance and Cancer. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9911-5.

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Capítulos de libros sobre el tema "Insulin resistance"

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Siddle, Ken. "The Insulin Receptor and Downstream Signalling". En Insulin Resistance, 1–62. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch1.

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Clarke, Daniel K. y Vidya Mohamed-Ali. "Adipokines and Insulin Resistance". En Insulin Resistance, 269–95. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch10.

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Krebs, Jeremy y Susan Jebb. "Dietary Factors and Insulin Resistance". En Insulin Resistance, 297–316. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch11.

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Wareham, Nicholas J., Søren Brage, Paul W. Franks y Rebecca A. Abbott. "Physical Activity and Insulin Resistance". En Insulin Resistance, 317–400. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch12.

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Argyropoulos, George, Steven Smith y Claude Bouchard. "Genetics of the Metabolic Syndrome". En Insulin Resistance, 401–50. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch13.

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Lamarche, Benoît y Jean-François Mauger. "Insulin Resistance and Dyslipidaemia". En Insulin Resistance, 451–66. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch14.

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Cleland, Stephen J. y John M. C. Connell. "Insulin Resistance, Hypertension and Endothelial Dysfunction". En Insulin Resistance, 467–83. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch15.

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Potau, Neus. "Insulin Resistance and Polycystic Ovary Syndrome". En Insulin Resistance, 485–509. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch16.

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Savage, David y Stephen O'Rahilly. "Syndromes of Severe Insulin Resistance (SSIRs)". En Insulin Resistance, 511–33. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch17.

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Randeva, Harpal S., Margaret Clarke y Sudhesh Kumar. "Therapeutic Strategies for Insulin Resistance". En Insulin Resistance, 535–60. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch18.

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Actas de conferencias sobre el tema "Insulin resistance"

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Goodwin, P. "Obesity, Insulin Resistance and Insulin." En Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-ms2-1.

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Al-Jaber, Hend Sultan, Layla Jadea Al-Mansoori y Mohamed Aghar Elrayess. "The Role of GATA3 in Adipogenesis & Insulin Resistance". En Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0143.

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Background: Impaired adipogenesis plays an important role in the development of obesityassociated insulin resistance and type 2 diabetes. Adipose tissue inflammation is a crucial mediator of this process. In hyperglycemia, immune system is activated partially through upregulation of GATA3, causing exacerbation of the inflammatory state associated with obesity. GATA3 also plays a role as a gatekeeper of terminal adipocyte differentiation. Here we are examining the impact of GATA3 inhibition in adipose tissue on restoring adipogenesis, reversing insulin resistance and potentially lowering the risk of type 2 diabetes. Results: GATA-3 expression was higher in insulin resistant obese individuals compared to their insulin sensitive counterparts. Targeting GATA-3 with GATA-3 specific inhibitors reversed impaired adipogenesis and induced changes in the expression of a number insulin signaling-related genes, including up-regulation of insulin sensitivity-related gene and down-regulation of insulin resistance-related genes. Conclusion: GATA3 expression is higher in differentiating adipocytes from obese insulin resistant. Inhibiting GATA3 improves adipocytes differentiation and rescues insulin sensitivity in insulin resistant cells
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Altuve, Miguel, Erika Severeyn y Sara Wong. "Unsupervised subjects classification using insulin and glucose data for insulin resistance assessment". En 2015 20th Symposium on Signal Processing, Images and Computer Vision (STSIVA). IEEE, 2015. http://dx.doi.org/10.1109/stsiva.2015.7330444.

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Christopher, Pretty,. "Corticosteroids and Insulin Resistance in the ICU". En Modeling and Control in Biomedical Systems, editado por Rees, Stephen, Chair Andreassen, Steen y Andreassen, Steen. Elsevier, 2009. http://dx.doi.org/10.3182/20090812-3-dk-2006.00005.

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"Genetic Variations in Women with Insulin Resistance". En International Institute of Chemical, Biological & Environmental Engineering. International Institute of Chemical, Biological & Environmental Engineering, 2015. http://dx.doi.org/10.15242/iicbe.c0615079.

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Aldali, Sara Haitham y Sownd Sankaralingam. "Induction of Glyoxalase 1 to prevent Methylglyoxal-Induced Insulin Resistance in Cardiomyocytes". En Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0230.

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Background: Type 2 Diabetes mellitus is characterized by hyperglycemia and insulin resistance. Methylglyoxal (MG) a highly reactive dicarbonyl compound is also increased in diabetes. MG is detoxified by glyoxalase 1 (Glo-1) enzyme using reduced glutathione (GSH) as a co-factor. MG has been shown to have deleterious effects on cardiovascular cells and impairs insulin signaling. Insulin resistance is associated with diabetic cardiomyopathy. Trans-resveratrol (tRES) and Hesperetin (HES) combination has been shown to increase Glo-1 and improve insulin signaling in obese patients. Aim(s): The aim of this study is to investigate whether tRES-HES combination prevents MG-induced cardiac insulin resistance and the underlying mechanisms in cardiomyocytes in culture. Methodology: (H9C2) rat cardiomyocytes were treated with MG (100 µM) for 24 hours in the presence or absence of tRES-HES (10 µM). Glo-1 activity was determined by the formation of S-D lactoylglutathione; protein expression of P-Akt and P-GSK3b was determined using Western blot. In some experiments, cells were stimulated with insulin (100 nM) for 10 minutes to test insulin sensitivity. Results: MG reduced Glo-1 activity by ~25%, blunted insulin-induced phosphorylation of Akt and Gsk3b and increased the expression of beta-myosin heavy chain by ~50% (a marker of cardiac dysfunction) significantly (P˂0.05) compared to untreated control group of cells. Co-administration of tRES-HES combination restored Glo1 activity, maintained insulin-induced phosphorylation of Akt and GSK3b and prevented the increase in beta myosin heavy chain significantly (P<0.05). Conclusion: Induction of Glo1 prevents MG-induced cardiac insulin resistance and the increase in marker of cardiac dysfunction. This strategy could be helpful in preventing cardiovascular complications associated with diabetes.
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Došenović, Marinković, Biljana Delić-Vujanović, Marko Cincović, Siniša Grubač y Radojica Đoković. "The relationship of glucose, insulin, NEFA and index of insulin resistance with the metabolic adaptation of cows in the period before and after calving". En Zbornik radova 26. medunarodni kongres Mediteranske federacije za zdravlje i produkciju preživara - FeMeSPRum. Poljoprivredni fakultet Novi Sad, 2024. http://dx.doi.org/10.5937/femesprumns24010d.

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Metabolic indicators of poor energy status of cows are: decreased glucose and insulin concentration and increased NEFA concentration with increased insulin resistance. This metabolic profile is characteristic of the peripartum period in cows and is caused by reduced food intake and increased glucose directing towards the mammary gland and the pregnant uterus. The aim of this research is to examine the differences in insulin resistance in cows in dry and early lactation and examine the relationship between indicators of insulin resistance and metabolic profile parameters in early lactation. A statistically significant correlation was obtained between metabolic parameters and indicators of insulin resistance, and these relationships are most pronounced in the postpartum period. The RQUICKI index has a very weak predictive value for metabolic parameters, while the values of insulin, glucose and NEFA have a significant predictive value for a large number of parameters. The values of NEFA and insulin in the antepartum period correlate with certain metabolic parameters, but the number of statistically significant correlations is significantly lower. The individual values of insulin, glucose and NEFA have a much more significant association with metabolic parameters compared to the RQUICKI index of insulin resistance, which is calculated from the three parameters.
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Forstner, Thomas, Christiane Dienhart, Ludmilla Kedenko, Gernot Wolkersdörfer y Bernhard Paulweber. "Models for Predicting the Development of Insulin Resistance". En 6th International Conference on Data Science, Technology and Applications. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0006344801210125.

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Abogamal, A., E. Mahmoud, S. Abdulhakiem, S. Abdelatif y A. Abdelaziz. "FRI0482 Insulin resistance in patients with psoriatic arthritis". En Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5165.

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Kawayama, Tomotaka, Tomomi Sekizuka, Kazuko Matsunaga, Tomoaki Hoshino y Hisamichi Aizawa. "Insulin Resistance Associated With Systemic Inflammation In COPD". En American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2610.

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Informes sobre el tema "Insulin resistance"

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Chen, Jiankun, Yingming Gu, Lihong Yin, Minyi He, Na Liu, Yue Lu, Changcai Xie, Jiqiang Li y Yu Chen. Network meta-analysis of curative efficacy of different acupuncture methods on obesity combined with insulin resistance. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, agosto de 2022. http://dx.doi.org/10.37766/inplasy2022.8.0075.

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Review question / Objective: Population：Patients diagnosed as obesity with insulin resistance. Obesity reference: Consensus of experts on the Prevention and treatment of adult obesity in China in 2011 and Consensus of Chinese experts on medical nutrition therapy for overweight/obesity in 2016 were developed by the Obesity Group of Chinese Society of Endocrinology(CSE); BMI≥28. IR reference: According to the Expert opinions on insulin resistance evaluation published by Chinese Diabetes Society, HOMA-IR≥2.68 is regarded as the standard for the diagnosis of IR. Regardless of age, gender and course of disease. Patients diagnosed as obesity with insulin resistance. Intervention：Any kind of acupuncture, moxibustion, acupuncture+moxibustion, warm acupuncture, electropuncture, auricular point, acupoint application and acupoint catgut embedding. Comparison：Other acupuncture treatments, Drug therapy or blank control. Outcome：Primary outcomes: ①Fasting blood-glucose (FBG); ②Fasting serum insulin (FINS); ③Homeostasis model assessment-IR (HOMA-IR); ④Body Mass Index (BMI). Secondary outcomes: ①Waistline; ②Waist-hip ratio;③Triglyceride (TG); ④Total cholesterol (TC); ⑤High-density lipoprotein (HDL); ⑥Low-density lipoprotein (LDL). Study: Randomized controlled trials (RCTs) of different acupuncture methods in the treatment on obesity with insulin resistance, blind method and language are not limited. Randomized controlled trials (RCTs).
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Malin, Alecia, Wei Zheng y Herbert Yu. Insulin Resistance, IGFs and Energy Balance on the Risk of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, mayo de 2002. http://dx.doi.org/10.21236/ada406834.

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Olefsky, Jerrold. Role of Inflammation and Insulin Resistance in Mouse Models of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, abril de 2013. http://dx.doi.org/10.21236/ada580520.

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Gao, Hui, Dan Chen y Miao Zang. Association between phthalate exposure and insulin resistance: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, abril de 2021. http://dx.doi.org/10.37766/inplasy2021.4.0026.

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Cai, Wangyu y Jian Xu. Insulin resistance in women with recurrent miscarriage: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, noviembre de 2021. http://dx.doi.org/10.37766/inplasy2021.11.0055.

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Gao, Hui, Chen Gong, Shi-chun Shen, Jia-ying Zhao, Dou-dou Xu, Fang-biao Tao, Yang Wang y Xiao-chen Fan. A systematic review on the associations between prenatal phthalate exposure and childhood glycolipid metabolism and blood pressure: evidence from epidemiological studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, junio de 2022. http://dx.doi.org/10.37766/inplasy2022.6.0111.

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Review question / Objective: The present systematic review was performed to obtain a summary of epidemiological evidence on the relationships of in utero exposure to phthalates with childhood glycolipid metabolism and blood pressure. Condition being studied: Childhood cardiovascular risk factors including blood pressure, lipid profile (e.g., triglycerides, total cholesterol, HDL−C, LDL−C) and glucose metabolism (e.g., insulin, insulin resistance, insulin sensitivity, glucose) were the interested outcomes. Eligibility criteria: In brief, epidemiological studies including cohort study, case-control study and cross-sectional survey were screened. Studies regarding relationships between human exposure to organophosphate esters and neurotoxicity were possible eligible for the present systematic review. The adverse neurodevelopmental outcomes included development of cognition, behavior, motor, brain change, emotion, etc. Studies that did not meet the above criteria were not included in this systematic review.
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Zhao, Junyu, Qianping Zhang, Yupeng Yang, Jinming Yao, Lin Liao y Jianjun Dong. High Prevalence of Thyroid Carcinoma in Patients with Insulin Resistance: A Meta-analysis of Case-control Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, agosto de 2021. http://dx.doi.org/10.37766/inplasy2021.8.0043.

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Miao, Chenyun, Qingge Guo, Xiaojie Fang, Yun Chen, Ying Zhao y Qin Zhang. Effects of Probiotics and Synbiotics Supplementation on Insulin Resistance in Women with Polycystic Ovary Syndrome: A Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, mayo de 2021. http://dx.doi.org/10.37766/inplasy2021.5.0112.

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Podgorski, Izabela. Biochemical and Genetic Markers in Aggressiveness and Recurrence of Prostate Cancer: Race-Specific Links to Inflammation and Insulin Resistance. Fort Belvoir, VA: Defense Technical Information Center, julio de 2012. http://dx.doi.org/10.21236/ada566642.

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HE, QINGQING y CHANGQIANG LI. The effect of isotretinoin in the treatment of acne vulgaris on insulin resistance: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, septiembre de 2021. http://dx.doi.org/10.37766/inplasy2021.9.0065.

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