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Gene Symbol |
INS |
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Aliases |
IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10 |
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Entrez Gene ID |
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Gene Name |
Insulin |
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Chromosomal Location |
11p15.5 |
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HGNC ID |
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Summary |
This gene encodes insulin, a peptide hormone that plays a vital role in the regulation of carbohydrate and lipid metabolism. After removal of the precursor signal peptide, proinsulin is post-translationally cleaved into three peptides: the B chain and A chain peptides, which are covalently linked via two disulfide bonds to form insulin, and C-peptide. Binding of insulin to the insulin receptor (INSR) stimulates glucose uptake. A multitude of mutant alleles with phenotypic effects have been identified. There is a read-through gene, INS-IGF2, which overlaps with this gene at the 5' region and with the IGF2 gene at the 3' region. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jan 2019]
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RefSeq DNA |
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RefSeq mRNA |
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e!Ensembl
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Gene Ontology (GO)
GO ID |
Ontology |
Function |
Evidence |
Reference |
GO:0002674 |
Biological process |
Negative regulation of acute inflammatory response |
IDA |
11443198 |
GO:0006355 |
Biological process |
Regulation of transcription, DNA-templated |
NAS |
12881524 |
GO:0006521 |
Biological process |
Regulation of cellular amino acid metabolic process |
IMP |
3553851 |
GO:0006953 |
Biological process |
Acute-phase response |
IDA |
14739855 |
GO:0007186 |
Biological process |
G protein-coupled receptor signaling pathway |
IDA |
9092559 |
GO:0007267 |
Biological process |
Cell-cell signaling |
IC |
7556975 |
GO:0008284 |
Biological process |
Positive regulation of cell proliferation |
IDA |
7688386, 17925406 |
GO:0008286 |
Biological process |
Insulin receptor signaling pathway |
IDA |
20455999 |
GO:0010628 |
Biological process |
Positive regulation of gene expression |
IGI |
25403480 |
GO:0010750 |
Biological process |
Positive regulation of nitric oxide mediated signal transduction |
IDA |
15792832 |
GO:0010750 |
Biological process |
Positive regulation of nitric oxide mediated signal transduction |
IMP |
14615391 |
GO:0014068 |
Biological process |
Positive regulation of phosphatidylinositol 3-kinase signaling |
IDA |
7688386 |
GO:0022898 |
Biological process |
Regulation of transmembrane transporter activity |
IDA |
14615391 |
GO:0030307 |
Biological process |
Positive regulation of cell growth |
NAS |
11742412 |
GO:0030335 |
Biological process |
Positive regulation of cell migration |
ISS |
12138094 |
GO:0031954 |
Biological process |
Positive regulation of protein autophosphorylation |
ISS |
3518947 |
GO:0032148 |
Biological process |
Activation of protein kinase B activity |
IDA |
8702995 |
GO:0032270 |
Biological process |
Positive regulation of cellular protein metabolic process |
IMP |
3553851 |
GO:0032460 |
Biological process |
Negative regulation of protein oligomerization |
IDA |
9830016 |
GO:0032880 |
Biological process |
Regulation of protein localization |
IDA |
14615391 |
GO:0033861 |
Biological process |
Negative regulation of NAD(P)H oxidase activity |
IDA |
11443198 |
GO:0042060 |
Biological process |
Wound healing |
IDA |
9498508 |
GO:0042177 |
Biological process |
Negative regulation of protein catabolic process |
IDA |
15185208 |
GO:0042593 |
Biological process |
Glucose homeostasis |
IMP |
381941 |
GO:0043410 |
Biological process |
Positive regulation of MAPK cascade |
IDA |
11500939, 20455999 |
GO:0045597 |
Biological process |
Positive regulation of cell differentiation |
NAS |
11742412 |
GO:0045721 |
Biological process |
Negative regulation of gluconeogenesis |
NAS |
11742412 |
GO:0045725 |
Biological process |
Positive regulation of glycogen biosynthetic process |
IDA |
17925406 |
GO:0045818 |
Biological process |
Negative regulation of glycogen catabolic process |
IMP |
381941 |
GO:0045821 |
Biological process |
Positive regulation of glycolytic process |
IDA |
7688386 |
GO:0045821 |
Biological process |
Positive regulation of glycolytic process |
IMP |
381941 |
GO:0045840 |
Biological process |
Positive regulation of mitotic nuclear division |
IDA |
10644978, 11500939 |
GO:0045861 |
Biological process |
Negative regulation of proteolysis |
IMP |
3553851 |
GO:0045922 |
Biological process |
Negative regulation of fatty acid metabolic process |
IMP |
1184755 |
GO:0046326 |
Biological process |
Positive regulation of glucose import |
IDA |
14615391, 15792832 |
GO:0046326 |
Biological process |
Positive regulation of glucose import |
IMP |
14615391 |
GO:0046628 |
Biological process |
Positive regulation of insulin receptor signaling pathway |
IDA |
7688386, 15792832 |
GO:0046628 |
Biological process |
Positive regulation of insulin receptor signaling pathway |
IMP |
14615391 |
GO:0046631 |
Biological process |
Alpha-beta T cell activation |
IDA |
10604997 |
GO:0046889 |
Biological process |
Positive regulation of lipid biosynthetic process |
NAS |
11742412 |
GO:0048167 |
Biological process |
Regulation of synaptic plasticity |
TAS |
19188609 |
GO:0050708 |
Biological process |
Regulation of protein secretion |
IDA |
15591776 |
GO:0050709 |
Biological process |
Negative regulation of protein secretion |
IDA |
14739855 |
GO:0050715 |
Biological process |
Positive regulation of cytokine secretion |
IDA |
15473891 |
GO:0050890 |
Biological process |
Cognition |
TAS |
19188609 |
GO:0050995 |
Biological process |
Negative regulation of lipid catabolic process |
IMP |
24675707 |
GO:0050995 |
Biological process |
Negative regulation of lipid catabolic process |
NAS |
11742412 |
GO:0051000 |
Biological process |
Positive regulation of nitric-oxide synthase activity |
NAS |
12135947 |
GO:0051092 |
Biological process |
Positive regulation of NF-kappaB transcription factor activity |
IDA |
19727662 |
GO:0051897 |
Biological process |
Positive regulation of protein kinase B signaling |
IDA |
11500939 |
GO:0055089 |
Biological process |
Fatty acid homeostasis |
IMP |
1184755 |
GO:0060266 |
Biological process |
Negative regulation of respiratory burst involved in inflammatory response |
IDA |
11443198 |
GO:0060267 |
Biological process |
Positive regulation of respiratory burst |
IDA |
9092559 |
GO:0090277 |
Biological process |
Positive regulation of peptide hormone secretion |
TAS |
11387233 |
GO:0090336 |
Biological process |
Positive regulation of brown fat cell differentiation |
TAS |
11387233 |
GO:0097755 |
Biological process |
Positive regulation of blood vessel diameter |
NAS |
14744991 |
GO:0097756 |
Biological process |
Negative regulation of blood vessel diameter |
NAS |
12946932 |
GO:1900182 |
Biological process |
Positive regulation of protein localization to nucleus |
IDA |
20455999 |
GO:1900273 |
Biological process |
Positive regulation of long-term synaptic potentiation |
TAS |
19188609 |
GO:1902176 |
Biological process |
Negative regulation of oxidative stress-induced intrinsic apoptotic signaling pathway |
NAS |
16604263 |
GO:1902952 |
Biological process |
Positive regulation of dendritic spine maintenance |
IGI |
19188609 |
GO:1903076 |
Biological process |
Regulation of protein localization to plasma membrane |
IGI |
19188609 |
GO:1903427 |
Biological process |
Negative regulation of reactive oxygen species biosynthetic process |
IGI |
19188609 |
GO:1990535 |
Biological process |
Neuron projection maintenance |
IGI |
19188609 |
GO:2000252 |
Biological process |
Negative regulation of feeding behavior |
IDA |
17957153 |
GO:0005576 |
Cellular component |
Extracellular region |
IC |
7556975 |
GO:0005615 |
Cellular component |
Extracellular space |
IDA |
9667398 |
GO:0002020 |
Molecular function |
Protease binding |
IPI |
20082125 |
GO:0005158 |
Molecular function |
Insulin receptor binding |
IDA |
7556975, 9667398 |
GO:0005158 |
Molecular function |
Insulin receptor binding |
IPI |
8452530 |
GO:0005159 |
Molecular function |
Insulin-like growth factor receptor binding |
IPI |
8452530 |
GO:0005179 |
Molecular function |
Hormone activity |
IC |
9667398 |
GO:0005179 |
Molecular function |
Hormone activity |
IMP |
381941 |
GO:0005179 |
Molecular function |
Hormone activity |
NAS |
14986111 |
GO:0005515 |
Molecular function |
Protein binding |
IPI |
9388210, 9773776, 17051221, 23302862 |
GO:0042802 |
Molecular function |
Identical protein binding |
IPI |
17472440, 20738396, 23106816, 23416304, 23510797 |
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Protein Information |
|
Protein Name |
Insulin, preproinsulin, proinsulin |
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Function |
Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver |
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UniProt |
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PDB |
3UTQ, 3UTS, 3UTT, 5C0D, 5HYJ, 4Y19, 4Y1A, 4WDI, 4Z76, 4Z77, 4Z78, 1JK8, 2G54, 2G56, 2WBY, 2WC0, 5CJO, 5WOB, 6B3Q, 6B70, 6BFC, 3W11, 3W12, 3W13, 4OGA, 6HN5, 1A7F, 1AI0, 1AIY, 1B9E, 1BEN, 1EFE, 1EV3, 1EV6, 1EVR, 1FU2, 1FUB, 1G7A, 1G7B, 1GUJ, 1HIQ, 1HIS, 1HIT, 1HLS, 1HTV, 1HUI, 1IOG, 1IOH, 1J73, 1JCA, 1JCO, |
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Pfam |
Pfam Accession |
Pfam ID |
PF00049 |
Insulin |
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Interactions |
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STRING |
MINT |
IntAct |
ENSP00000399421 |
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P16671 |
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View interactions
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Associated Diseases
Disease group | Disease Name | References |
Cardiovascular Diseases |
Heart Failure |
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Ventricular Outflow Obstruction |
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Cardiomyopathy |
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Cardiac Arrest |
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Hypertensive disease |
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Diabetic Cardiomyopathies |
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Myocardial Failure |
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Ventricular Fibrillation |
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Congenital, Hereditary, and Neonatal Diseases and Abnormalities |
Diastematomyelia |
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Primary tethered cord syndrome |
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Atonic seizures |
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Anencephaly |
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Neurenteric Cyst |
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Developmental Delay, Epilepsy, and Neonatal Diabetes |
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Status Dysraphicus |
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22q13.3 Deletion Syndrome |
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Digestive System Diseases |
Fatty Liver |
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Hepatitis |
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Pancreatitis |
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Liver Failure |
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Endocrine System Diseases |
Diabetes Mellitus |
15628829, 7624867, 7294224, 8400068, 18162506, 11446671, 17855560, 2055425, 21779873, 3511099, 11522680, 11978674, 16259526, 21680998, 16519038, 7573102, 15531508, 23349674, 25751624, 21829393, 20620209 |
MODY |
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Ketosis-prone diabetes |
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Diabetes Insipidus |
18162506, 17855560, 25741868, 26101329, 20938745, 18451997, 17047922, 18171712, 20301620, 18414213, 18192540 |
Monogenic Diabetes |
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Glomerulosclerosis |
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Diabetic Ketoacidosis |
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Brittle diabetes |
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PCOS |
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Insulin Resistance Syndrome |
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Immune System Diseases |
Autoimmune Diabetes |
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Musculoskeletal Diseases |
Myopathy |
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Neoplasms |
Prostate cancer |
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Ovarian Cancer |
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Nervous System Diseases |
Seizures |
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MPTP-Induced Degeneration of the Striatum |
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Diabetes Mellitus, permanent neonatal, with neurologic features |
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Parkinson Disease |
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Jacksonian Seizure |
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Neural Tube Defects |
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Nutritional and Metabolic Diseases |
Hyperproinsulinemia |
6382002, 6368587, 7350438, 3470784, 8636380, 381941, 9667398, 7242673, 3537011, 1601997, 3511099, 6261753, 3306677, 2991050, 9141561, 3057496, 4019786, 6339950, 6312455, 8421693, 6371526, 2196279 |
Hypoglycemia |
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Hyperinsulinism |
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Metabolic Syndrome X |
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Metabolic Diseases |
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Obesity |
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Hyperglycemia |
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Gluocose Intolerance |
30448542, 27669460, 27323669, 28223291, 15220191, 18339976, 28453960, 19140314, 22507373, 22226490, 9544854, 11679606, 16380496, 29537219, 17617923, 18269634, 19087913, 23637927, 23094072, 17143606, 18842181, 23688034, 11887173, 10751748, 19401444, 23640882, 19553674 |
Psychiatric/Brain disorders |
Senile Dementia |
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Delirium, Dementia, Amnestic, Cognitive Disorders |
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Mental Depression |
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Mental disorders |
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Alzheimer Disease |
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Bipolar Disorder |
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Manic Disorder |
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Psychosis |
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Lewy Body Disease |
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Memory Disorders |
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Panic Attacks |
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Neurocognitive Disorders |
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Kandinsky Syndrome |
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Panic Disorder |
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Organic Brain Syndrome, Nonpsychotic |
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Obstructive Sleep Apnea |
26201496, 26941371, 29968150, 28219664, 25944984, 26657991, 22451332, 24410986, 17202301, 21664182, 20405330, 14521752, 19251800, 23524009, 21669017 |
Renal Disorder |
Kidney Insufficiency |
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Kidney Failure |
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Diabetic Nephropathy |
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Polycystic Kidney Diseases |
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Urinary Bladder Diseases |
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Reproductive disorders |
Preeclampsia |
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References |
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PubMed ID |
Associated gene/s |
Associated condition |
Genetic Mutation |
Diagnostic Criteria |
Association with PCOS |
Ethnicity |
Conclusion |
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Obesity |
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Related
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21 obese women with PCO, 18 obese women without menstrual disturbances and 9 normal-weight healthy women |
obese women with PCO insulin influence ovarian androgen production |
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Androgen and IGFBPs |
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Related
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Women undergoing IVF for tubal disease |
Androgen and insulin are important regulators of IGFBP release and that elevated levels of the two hormones may contribute to the altered IGFBP profile found in PCOS follicles |
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Androgen and CD(36) |
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Related
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12 patients with asymmetric PCO, 15 primary or secondary infertile patients without endocrine disorders and 8 PCOS with bilateral PCO were recruited |
Decrease of scavenger receptor gene CD(36) mRNA may play a role in the pathogenesis of PCO by increasing the level of T and INSin follicular fluid. |
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TNF-alpha |
Hyperinsulinaemia |
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Related
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20 young non-diabetic women with PCOS and 21 control |
The decrease in TNF-alpha concentrations during oGTT and the inverse correlation between endogenous hyperinsulinaemia and serum TNF-alpha concentrations suggested an anti-inflammatory effect of moderately-high insulin concentrations. This occurred despite the presence of moderate hyperglycaemia. These findings also demonstrated a preserved responsiveness of inflammatory mediators to insulin in PCOS. |
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GH and Glucose |
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Rotterdam criteria |
Related
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20 obese women with PCOS, and 15 obese controls. |
The injection of ghrelin seems to override the GH secretion defect in obese women with PCOS, and to induce glucoinsulinemic changes in both controls and obese patients with PCOS. |
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TCM and Sex Hormone |
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Related
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120 patients with PCOS were determined |
Level of T, LH and LH/FSH ratio, PRL and INS are correlated with the TCM syndrome in patients with PCOS |
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Androgen |
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Related
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48 patients with non-diabetic PCOS and compare with a non-PCOS group of 30 subjects |
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GnRH |
Hyperinsulinemia |
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Rotterdam criteria, NIH criteria |
Related
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9 young PCOS women participated in the study |
Sustained hyperinsulinemia potentiates gonadotropin-stimulated ovarian androgen steroidogenesis. |
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Direct
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1075 PCOS patients and 2878 controls |
Meta-analysis suggests that the III allele of INS VNTR is associated with increased risk of PCOS |
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The inclusion criteria were as follows: (1) casecontrol or cohort studies design with evaluating the association between PCOS risk andINSVNTR polymorphism; (2) PCOS patients with any diagnosis criteria; the anovulation of anovulatory PCOS was defined a |
Direct
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1767 cases, 4108 controls |
Meta-analysis supports that the III allele of INS VNTR is associated with susceptibility to PCOS |
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INS-VNTR polymorphism |
Rotterdam criteria |
Direct
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PCR-RFLP in 216 PCOS patients and 192 non-PCOS women as a control group. |
No association with PCOS |
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Glucose |
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Related
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20 PCOS women with normal glucose tolerance and 20 age-matched healthy women |
PCOS womens show significant decrease of peripheral insulin sensitivity with compensated increase of insulin secretion. |
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Testosterone |
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Related
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97 PCOS patients,50 being non-obese, and 27 women with oviductal sterility (control group) |
The difference in homeostasis ability to T and insulin may be related to the difference in the various parameters |
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LH |
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Patients diagnosed with PCOS on the basis of amenorrhea and a polycystic morphology at ovarian ultrasound |
Related
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5 nonobese patients diagnosed with PCOS and 5 normal control |
Insulin can modulate the activity of hypothalamic GnRH neurons in the humans |
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LH and GnRH |
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NIH criteria |
Related
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18 PCOS and 21 normal women |
In PCOS, insulin infusion suppresses pituitary response to GnRH. In normal women, insulin negatively correlates with mean LH and suppresses GnRH response at a high infusion rate. |
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lipoprotein |
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Rotterdam criteria |
Related
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299 Women with polycystic ovary syndrome and 187 control womens from European Society of Human Reproduction and Embryology |
Polymorphism of C/T in the low-density lipoprotein receptor-related protein-5 gene is associated with C-peptide and proinsulin secretion but does not influence insulin |
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Hyperandrogenemia |
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Polycystic ovary syndrome was defined by oligomenorrhea (8 menstrual periods in the preceding year) or confirmed anovulation, and hyperandrogenemia |
Related
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9 lean womenwith PCOS and normal insulin levels, as well as 17 lean healthy women |
women with typical PCOS and normal insulin levels and metabolic insulin sensitivity, reducing insulin secretion significantly decreased androgen and increased SHBG levels |
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IGFs |
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Rotterdam criteria |
Related
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6 PCOS and 6 non-PCOS women undergoing COS and IVF |
Insulin and IGFs promote VEGF-A production in LGCs, but the response patterns are different when cells from PCOS and non-PCOSwomen are compared. |
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INS-VNTR gene |
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Rotterdam criteria |
Direct
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255 parent-offspring trios,185 additional cases and 1062 control subjects as well as 1599 women from a northern Finland population |
Despite the strong biological candidacy and supportive data from previous studies, we conclude that variation at the INS-VNTR has no major role in the development of PCOS. |
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LH/FSH |
Hyperinsulinemia |
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Related
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119 polycystic ovary syndrome women in reproductive age |
Most of the PCOS women with normal gonadotropin ratio belong to a group of patients suffering from hyperinsulinemia and obesity |
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C-peptide |
Hyperinsulinemia |
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The diagnosis of PCOS was based on the presence ofthree or more of the following features: luteinizing hormone(LH): follicle stimulating hormone (FSH) ratio > 2.5, highlevels of total testosterone (total T), free testosterone (free T),androstenedione |
Related
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63 patients with normal body mass index were included: 48 had clinical and hormonal features of PCOS and 15 were normo-ovulatory |
Insulin and C-peptide do not seem to interfere with uterine perfusion in PCOS-affected patients |
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Hyperinsulinism, Dyslipidaemia and Hyperandrogenism |
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Related
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51 girls with a history of PP and compared normal-birthweight (n = 26) with low-birthweight (n = 25) girls |
The longitudinal data show that, in PP girls, the endocrine-metabolic risk conferred by prenatal growth restraint is not readily detectable until puberty or postmenarche, and is not attributable to a higher body mass index. |
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Insulin secretion |
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NIH criteria |
Related
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women with PCOS (n = 33) and their nondiabetic first degree relatives (n = 48) |
Heritability of beta-cell dysfunction is likely to be a significant factor in the predisposition to diabetes in PCOS |
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Beta-endorphin |
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Related
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167 subjects with PCOD were recruited, 117 of whom had normal weight |
Stratified and linear regression analysis showed that plasma beta-endorphin concentrations correlate more with BMI than with insulinemia |
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LH and Androgen |
Hyperandrogenism and Hyperinsulinemia |
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Related
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58 adolescents with regular menstrual cycles, 50 with irregular menstrual cycles, and 29 with oligomenorrhea |
It is doubtful that hyperinsulinemia is an important factor in the development of PCO or polycystic ovary syndrome |
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INS VNTR gene |
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Related
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31 healthy adult subjects with normal glucose tolerance. 17 subjects were homozygous for class I alleles and 14 homozygous for class III alleles |
further analysis of possible association between allelic variation of the INS VNTR and the pulsatility of insulinsecretion |
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Androgens |
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PCOS was diagnosed on the basis of hyperandrogenism and chronic anovulation after the exclusion of tumors, Cushings syndrome, and adrenal enzymatic deficiencies based on measurements of cortisol and 17OH progesterone, respectively. |
Related
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21 women with PCOS of normal body weight, 8 apparently normal women with PAO and 21 normal women. |
Normal weight patients serum leptin levels may be regulated in part by insulin. Androgens, on the other hand, may play a role in suppressing serum leptin |
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Hyperinsulinemic |
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Related
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normoinsulinemic-lean =24, normoinsulinemic obese = 24, hyperinsulinemic lean= 17, hyperinsulinemic obese = 45 |
independent and synergistic additive effect of obesity and hyperinsulinemia on the FAI in PCOS |
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GnRH-analog |
hyperandrogenism, hyperinsulinism and acanthosis nigricans |
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Related
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6 patients with clinical findings of PCO, hirsutism and acanthosis nigricans |
Hirsutism and acanthosis nigricans present high levels of insulin, suggesting an ovarian hyperesponsiveness, which is not sustained when gonadotrophic blockage was achieved |
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IGF-I receptors |
Hyperandrogenism and Hyperinsulinaemia |
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Related
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10 women with PCOS and 8normo-ovulatory women |
Number of IGF-I receptors and not the insulin levels correlate with serum androstenedione |
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FSH |
Hyperinsulinemia |
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PCOS was diagnosed on the basis of all these criteria: clinical findings (presence of amenorrhea or oligomenorrhea and hirsutism), elevated plasma androgen levels (normal values: androstenedione (A) 2.07.0 nmol/L, testosterone (T) 0.62.0 nmol/L), and bi |
Related
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34 patients affected by PCOS |
In PCOS, the insulinemic pattern may influence the ovarian response to gonadotropin administration |
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Hyperinsulinemia |
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All proband cases met the criteria of polycystic ovaries (PCO) by ultrasound (US) and hyperandrogenism. |
Related
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Family members of PCOS subjects |
Hyperinsulinemia is a potential metabolic and genetic marker for subjects who may be carriers of a familial tendency for PCO |
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Hyperinsulinemia |
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Related
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240 PCOS womens(142 of the women were insulin resistant or hyperinsulinemic and 98 were normoinsulinemic) |
The hyperinsulinemic group had significantly higher plasma levels of androstenedione, testosterone, free testosterone and insulin, and lower levels of luteinizing hormone, estradiol and sex hormone-binding globulin. |
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Hyperinsulinaemia |
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Related
|
7 normal weight women with PCOS and 8 healthy women |
Hyperproinsulinaemia is modest and appropriate in PCOS, GIP and GLP-1(7-36) amide do not contribute to the stimulated hyperinsulinaemia in PCOS |
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Hyperinsulinemia and Androgen Excess |
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Related
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PCOS womens (LH/FSH (LH/FSH > or = 3 Group 1n=30 and LH/FSH<3 Group 2 n=25) |
Hyperinsulinemia in PCOS is due to a enhanced beta-cell secretion and an impaired hepatic clearance of this hormone, hyperandrogenism may be LH-dependent in Group 1 and insulin-dependent in Group 2 |
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Cardiovascular disease |
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Related
|
Twenty-six young women with PCOS and 11 healthy age matched women with regular ovulatory cycles |
An inverse relation between serum fasting insulin level and left ventricular systolic outflow parameters suggests that insulin is associated with the decreased systolic flow velocity observed in women with PCOS. |
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Hyperinsulinemia |
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Related
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13 healthy ovulatory women (group 1) and 6 women with PCOS and hyperinsulinemia,3with acanthosis nigricans (group 2) |
In conclusion, in PCOS women no parallel changes in serum androgen concentrations were seen in association with acute truly physiologic endogenous hyperinsulinemia or during the acute pharmacologically induced hypoinsulinemia and subsequent hyperinsulinemia. |
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OGTT |
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Related
|
8 normal and 29 anovulatory women (8 with multifollicular ovaries and 21 with PCOs) |
Insulin AUC was increased in both multifollicular ovary and PCO patients |
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Hyperinsulinemia |
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Related
|
20 hyperinsulinemic and 20 relatively nonhyperinsulinemic nondiabetic Pima women 18 to 45 years of age |
The association of obesity, hyperinsulinemia, irregular menstruation, and high testosterone concentration described in the PCO also occurs in Pima Indian women |
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LH andSHBG |
Hyperandrogenemia |
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Related
|
25 consecutive women with PCOS and 20 control women matched for BMI |
The data are consistent with the hypothesis that hyperinsulinemia in PCOS influences the biologically active component of T by lowering SHBG concentrations while having little apparent impact on LH-induced secretion of androgens in vivo. |
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Hyperinsulinaemic |
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Related
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102 women with ultrasound diagnosed PCOS and 19 lean women with normal ovaries were studied |
Hyperinsulinaemic women with PCOS have an increased risk of developing cardiovascular disease and therefore form a population in whom metabolic screening is advisable. |
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DHEAS |
Hyperinsulinemia |
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Related
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10 women with PCOD (5 obese and 5 normal weight) and 10 ovulatory euandrogenic women (5 obese and 5 normal-weight) |
Acute increases in insulin within the physiological range are important in the regulation of circulating DHEAS in either PCOD or euandrogenic women |
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Hyperinsulinemia |
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Related
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49 womens:27 women with PCO (9 obese and 18 nonobese), and 22 healthy women (12 with simple obesity and 10 with normal body weight) |
Hyperinsulinemia may play a role in the development of lipid disturbances in women with the PCO |
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diazoxide (100 mg, three times daily) administration |
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Related
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5 obese women with polycystic ovary syndrome was assessed on two occasions: before and after 10 days of oral diazoxide |
Hyperinsulinemia in obese women with polycystic ovary syndrome may directly increase serum testosterone levels |
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hyperandrogenism and hyperinsulinism |
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Related
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14 obese women: 8 with polycystic ovarian disease (PCOD) and 6 obese controls |
Hyperandrogenism correlates with hyperinsulinism |
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Leptin and Adiponectin |
Hyperinsulinemia |
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Related
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Insulin,leptin,adiponectin,cholesterol,triglyceride,A/L and L/A ratios were compared in women with PCOS and controls |
Insulin, L/A, and A/L ratios seem to be the best markers to distinguish women with and without PCOS. |
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AMH |
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Related
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135 PCOSd and 93 Cd classified according to their Tanner stage |
AMH value for the Cd group showed decreased FSH concentrations and increased stimulated levels of insulin |
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Related
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25 PCOS patients (13 were obese and 12 non-obese) |
PCOS there is a significant degree of hyperinsulinaemia which is mainly related to obesity |
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Androgen, ACTH |
Hyperinsulinemia |
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Related
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6 healthy ovulatory control women (Group 1) were compared against 7 women PCOS and hyperinsulinism |
The results suggest a certain degree of adrenal participation in the pathogenesis of the hyperandrogenism in these women, which may be the final expression of a synergistic stimulation of the adrenals by hyperinsulinism, relatively high LH, and chronic hyperestrogenism, all of which are present virtually in all women with PCOS. |
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CP450c17A,17-OHP , GnRH |
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Related
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28 women with PCOS and 18 normal women were included |
Hyperinsulinism may not play a role in the dysregulation of the cytochrome P450c17 alpha enzyme seen in PCOS |
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IGF-1 |
Hyperandrogenism and Hyperinsulinaemia |
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Related
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48 patients with PCOS and 10 women with normal weight and menstruation were recruited as controls |
INS may play an important role in hyperandrogenism by upregulating IGF-1 system in ovary |
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