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Impaired glucose tolerance

MedGen UID:
852424
Concept ID:
C0151671
Finding
Synonyms: Decreased glucose tolerance; Glucose tolerance decreased
 
HPO: HP:0040270

Definition

An abnormal resistance to glucose, i.e., a reduction in the ability to maintain glucose levels in the blood stream within normal limits following oral or intravenous administration of glucose. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVImpaired glucose tolerance

Conditions with this feature

Pituitary dependent hypercortisolism
MedGen UID:
66381
Concept ID:
C0221406
Disease or Syndrome
AIP familial isolated pituitary adenoma (AIP-FIPA) is defined as the presence of an AIP germline pathogenic variant in an individual with a pituitary adenoma (regardless of family history). The most commonly occurring pituitary adenomas in this disorder are growth hormone-secreting adenomas (somatotropinoma), followed by prolactin-secreting adenomas (prolactinoma), growth hormone and prolactin co-secreting adenomas (somatomammotropinoma), and nonfunctioning pituitary adenomas (NFPA). Rarely TSH-secreting adenomas (thyrotropinomas) are observed. Clinical findings result from excess hormone secretion, lack of hormone secretion, and/or mass effects (e.g., headaches, visual field loss). Within the same family, pituitary adenomas can be of the same or different type. Age of onset in AIP-FIPA is usually in the second or third decade.
Renal cysts and diabetes syndrome
MedGen UID:
96569
Concept ID:
C0431693
Disease or Syndrome
The 17q12 recurrent deletion syndrome is characterized by variable combinations of the three following findings: structural or functional abnormalities of the kidney and urinary tract, maturity-onset diabetes of the young type 5 (MODY5), and neurodevelopmental or neuropsychiatric disorders (e.g., developmental delay, intellectual disability, autism spectrum disorder, schizophrenia, anxiety, and bipolar disorder). Using a method of data analysis that avoids ascertainment bias, the authors determined that multicystic kidneys and other structural and functional kidney anomalies occur in 85% to 90% of affected individuals, MODY5 in approximately 40%, and some degree of developmental delay or learning disability in approximately 50%. MODY5 is most often diagnosed before age 25 years (range: age 10-50 years).
Islet cell adenomatosis
MedGen UID:
293643
Concept ID:
C1578917
Neoplastic Process
Insulinomatosis and diabetes mellitus syndrome is an autosomal dominant disorder in which affected individuals within a family present with either hyperinsulinemic hypoglycemia secondary to pancreatic neuroendocrine tumors, or a noninsulin-dependent form of diabetes mellitus. A few affected individuals show only impaired glucose tolerance. Some patients also exhibit congenital cataract and/or congenital glaucoma (Iacovazzo et al., 2018).
Hemochromatosis type 4
MedGen UID:
340044
Concept ID:
C1853733
Disease or Syndrome
Hemochromatosis type 4 (HFE4) is a dominantly inherited iron overload disorder with heterogeneous phenotypic manifestations that can be classified into 2 groups. One group is characterized by an early rise in ferritin (see 134790) levels with low to normal transferrin (190000) saturation and iron accumulation predominantly in macrophages. The other group is similar to classical hemochromatosis, with high transferrin saturation and prominent parenchymal iron loading (summary by De Domenico et al., 2005). For general background information and a discussion of genetic heterogeneity of hereditary hemochromatosis, see 235200.
Progressive external ophthalmoplegia with mitochondrial DNA deletions, autosomal dominant 4
MedGen UID:
350480
Concept ID:
C1864668
Disease or Syndrome
Progressive external ophthalmoplegia-4 is an autosomal dominant form of mitochondrial disease that variably affects skeletal muscle, the nervous system, the liver, and the gastrointestinal tract. Age at onset ranges from infancy to adulthood. The phenotype ranges from relatively mild, with adult-onset skeletal muscle weakness and weakness of the external eye muscles, to severe, with a multisystem disorder characterized by delayed psychomotor development, lactic acidosis, constipation, and liver involvement (summary by Young et al., 2011). For a general phenotypic description and a discussion of genetic heterogeneity of autosomal dominant progressive external ophthalmoplegia, see PEOA1 (157640).
Coronary artery disease, autosomal dominant 2
MedGen UID:
370259
Concept ID:
C1970440
Disease or Syndrome
Any coronary artery disease in which the cause of the disease is a mutation in the LRP6 gene.
Wolfram-like syndrome
MedGen UID:
481988
Concept ID:
C3280358
Disease or Syndrome
Autosomal dominant Wolfram-like syndrome (WFSL) is characterized by the clinical triad of congenital progressive hearing impairment, diabetes mellitus, and optic atrophy. The hearing impairment, which is usually diagnosed in the first decade of life, is relatively constant and alters mainly low- and middle-frequency ranges (summary by Valero et al., 2008). Wolfram syndrome (WFS1; 222300) is an autosomal recessive allelic disorder characterized by optic atrophy, diabetes mellitus, hearing loss, and diabetes insipidus, and is caused by homozygous or compound heterozygous mutation in the WFS1 gene. An autosomal dominant syndrome involving optic atrophy with or without deafness, ophthalmoplegia, myopathy, ataxia, and neuropathy (125250), is caused by heterozygous mutation in the OPA1 gene (605290).
Microcephaly-cerebellar hypoplasia-cardiac conduction defect syndrome
MedGen UID:
482322
Concept ID:
C3280692
Disease or Syndrome
The Zaki-Gleeson syndrome is an autosomal recessive neurodevelopmental disorder characterized by profound mental retardation, severe microcephaly, poor growth, cerebellar hypoplasia, and second-degree cardiac conduction defects (Zaki et al., 2011).
Partial lipodystrophy, congenital cataracts, and neurodegeneration syndrome
MedGen UID:
813897
Concept ID:
C3807567
Disease or Syndrome
Lipodystrophies are rare disorders characterized by loss of body fat from various regions and predisposition to metabolic complications of insulin resistance and lipid abnormalities. FPLD7 is an autosomal dominant disorder with a highly variable phenotype. Additional features, including early-onset cataracts and later onset of spasticity of the lower limbs, have been noted in some patients (summary by Garg et al., 2015). For a general phenotypic description and a discussion of genetic heterogeneity of familial partial lipodystrophy (FPLD), see 151660.
Estrogen resistance syndrome
MedGen UID:
815580
Concept ID:
C3809250
Disease or Syndrome
Estrogen resistance (ESTRR) is characterized by absence of puberty with elevated estradiol and gonadotropic hormones, as well as markedly delayed bone maturation. Female patients show absent breast development, small uterus, and enlarged multicystic ovaries; male patients may show small testes (Bernard et al., 2017). Some patients exhibit continued growth into adulthood (Smith et al., 1994).
Short-rib thoracic dysplasia 10 with or without polydactyly
MedGen UID:
816505
Concept ID:
C3810175
Disease or Syndrome
Short-rib thoracic dysplasia (SRTD) with or without polydactyly refers to a group of autosomal recessive skeletal ciliopathies that are characterized by a constricted thoracic cage, short ribs, shortened tubular bones, and a 'trident' appearance of the acetabular roof. SRTD encompasses Ellis-van Creveld syndrome (EVC) and the disorders previously designated as Jeune syndrome or asphyxiating thoracic dystrophy (ATD), short rib-polydactyly syndrome (SRPS), and Mainzer-Saldino syndrome (MZSDS). Polydactyly is variably present, and there is phenotypic overlap in the various forms of SRTDs, which differ by visceral malformation and metaphyseal appearance. Nonskeletal involvement can include cleft lip/palate as well as anomalies of major organs such as the brain, eye, heart, kidneys, liver, pancreas, intestines, and genitalia. Some forms of SRTD are lethal in the neonatal period due to respiratory insufficiency secondary to a severely restricted thoracic cage, whereas others are compatible with life (summary by Huber and Cormier-Daire, 2012 and Schmidts et al., 2013). There is phenotypic overlap with the cranioectodermal dysplasias (Sensenbrenner syndrome; see CED1, 218330). For a discussion of genetic heterogeneity of short-rib thoracic dysplasia, see SRTD1 (208500).
Seckel syndrome 10
MedGen UID:
934614
Concept ID:
C4310647
Disease or Syndrome
Any Seckel syndrome in which the cause of the disease is a mutation in the NSMCE2 gene.
Proteasome-associated autoinflammatory syndrome 1
MedGen UID:
1648310
Concept ID:
C4746851
Disease or Syndrome
Proteasome-associated autoinflammatory syndrome-1 (PRAAS1) is an autosomal recessive disorder characterized by early childhood onset of annular erythematous plaques on the face and extremities with subsequent development of partial lipodystrophy and laboratory evidence of immune dysregulation. More variable features include recurrent fever, severe joint contractures, muscle weakness and atrophy, hepatosplenomegaly, basal ganglia calcifications, and microcytic anemia (summary by Agarwal et al., 2010; Kitamura et al., 2011; Arima et al., 2011). This disorder encompasses Nakajo-Nishimura syndrome (NKJO); joint contractures, muscular atrophy, microcytic anemia, and panniculitis-induced lipodystrophy (JMP syndrome); and chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature syndrome (CANDLE). Among Japanese patients, this disorder is best described as Nakajo-Nishimura syndrome, since both Nakajo (1939) and Nishimura et al. (1950) contributed to the original phenotypic descriptions. Genetic Heterogeneity of Proteasome-Associated Autoinflammatory Syndrome See also PRAAS2 (618048), caused by mutation in the POMP gene (613386) on chromosome 13q12; PRAAS3 (617591), caused by mutation in the PSMB4 gene (602177) on chromosome 1q21; PRAAS4 (619183), caused by mutation in the PSMG2 gene (609702) on chromosome 18p11; PRAAS5 (619175), caused by mutation in the PSMB10 gene (176847) on chromosome 16q22; and PRAAS6 (620796), caused by mutation in the PSMB9 gene (177045) on chromosome 6p21.
Mandibuloacral dysplasia with type A lipodystrophy
MedGen UID:
1757618
Concept ID:
C5399785
Disease or Syndrome
Mandibuloacral dysplasia with type A lipodystrophy (MADA) is an autosomal recessive disorder characterized by growth retardation, craniofacial anomalies with mandibular hypoplasia, skeletal abnormalities with progressive osteolysis of the distal phalanges and clavicles, and pigmentary skin changes. The lipodystrophy is characterized by a marked acral loss of fatty tissue with normal or increased fatty tissue in the neck and trunk. Some patients may show progeroid features. Metabolic complications can arise due to insulin resistance and diabetes (Young et al., 1971; Simha and Garg, 2002; summary by Garavelli et al., 2009). See also MAD type B (MADB; 608612), which is caused by mutation in the ZMPSTE24 gene (606480).

Professional guidelines

PubMed

Beulens J, Rutters F, Rydén L, Schnell O, Mellbin L, Hart HE, Vos RC
Eur J Prev Cardiol 2019 Dec;26(2_suppl):47-54. doi: 10.1177/2047487319880041. PMID: 31766914
Garvey WT, Mechanick JI, Brett EM, Garber AJ, Hurley DL, Jastreboff AM, Nadolsky K, Pessah-Pollack R, Plodkowski R; Reviewers of the AACE/ACE Obesity Clinical Practice Guidelines
Endocr Pract 2016 Jul;22 Suppl 3:1-203. Epub 2016 May 24 doi: 10.4158/EP161365.GL. PMID: 27219496
Pippitt K, Li M, Gurgle HE
Am Fam Physician 2016 Jan 15;93(2):103-9. PMID: 26926406

Recent clinical studies

Etiology

Ziegler D, Herder C, Papanas N
Diabetes Metab Res Rev 2023 Nov;39(8):e3693. Epub 2023 Jul 20 doi: 10.1002/dmrr.3693. PMID: 37470302
Wu H, Tremaroli V, Schmidt C, Lundqvist A, Olsson LM, Krämer M, Gummesson A, Perkins R, Bergström G, Bäckhed F
Cell Metab 2020 Sep 1;32(3):379-390.e3. Epub 2020 Jul 10 doi: 10.1016/j.cmet.2020.06.011. PMID: 32652044
Priya G
J Pak Med Assoc 2018 Apr;68(4):669-671. PMID: 29808066
Brannick B, Dagogo-Jack S
Endocrinol Metab Clin North Am 2018 Mar;47(1):33-50. doi: 10.1016/j.ecl.2017.10.001. PMID: 29407055Free PMC Article
Huang Y, Cai X, Mai W, Li M, Hu Y
BMJ 2016 Nov 23;355:i5953. doi: 10.1136/bmj.i5953. PMID: 27881363Free PMC Article

Diagnosis

Ziegler D, Herder C, Papanas N
Diabetes Metab Res Rev 2023 Nov;39(8):e3693. Epub 2023 Jul 20 doi: 10.1002/dmrr.3693. PMID: 37470302
Echouffo-Tcheugui JB, Selvin E
Annu Rev Public Health 2021 Apr 1;42:59-77. Epub 2021 Dec 23 doi: 10.1146/annurev-publhealth-090419-102644. PMID: 33355476Free PMC Article
Rendell M
Expert Opin Pharmacother 2021 Jan;22(1):45-54. Epub 2020 Sep 7 doi: 10.1080/14656566.2020.1817381. PMID: 32892663
Wilson ML
Nurs Clin North Am 2017 Dec;52(4):665-677. Epub 2017 Oct 5 doi: 10.1016/j.cnur.2017.07.011. PMID: 29080583
Davies MJ, Gray IP
BMJ 1996 Feb 3;312(7026):264-5. doi: 10.1136/bmj.312.7026.264. PMID: 8611769Free PMC Article

Therapy

Hostalek U, Campbell I
Curr Med Res Opin 2021 Oct;37(10):1705-1717. Epub 2021 Jul 28 doi: 10.1080/03007995.2021.1955667. PMID: 34281467
Echouffo-Tcheugui JB, Selvin E
Annu Rev Public Health 2021 Apr 1;42:59-77. Epub 2021 Dec 23 doi: 10.1146/annurev-publhealth-090419-102644. PMID: 33355476Free PMC Article
Lips P, Eekhoff M, van Schoor N, Oosterwerff M, de Jongh R, Krul-Poel Y, Simsek S
J Steroid Biochem Mol Biol 2017 Oct;173:280-285. Epub 2016 Dec 5 doi: 10.1016/j.jsbmb.2016.11.021. PMID: 27932304
Garvey WT, Mechanick JI, Brett EM, Garber AJ, Hurley DL, Jastreboff AM, Nadolsky K, Pessah-Pollack R, Plodkowski R; Reviewers of the AACE/ACE Obesity Clinical Practice Guidelines
Endocr Pract 2016 Jul;22 Suppl 3:1-203. Epub 2016 May 24 doi: 10.4158/EP161365.GL. PMID: 27219496
Ríos JL, Francini F, Schinella GR
Planta Med 2015 Aug;81(12-13):975-94. Epub 2015 Jul 1 doi: 10.1055/s-0035-1546131. PMID: 26132858

Prognosis

Vounzoulaki E, Khunti K, Abner SC, Tan BK, Davies MJ, Gillies CL
BMJ 2020 May 13;369:m1361. doi: 10.1136/bmj.m1361. PMID: 32404325Free PMC Article
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Curr Vasc Pharmacol 2020;18(2):104-109. doi: 10.2174/1570161117666190405165911. PMID: 30961501
Gong Q, Zhang P, Wang J, Ma J, An Y, Chen Y, Zhang B, Feng X, Li H, Chen X, Cheng YJ, Gregg EW, Hu Y, Bennett PH, Li G; Da Qing Diabetes Prevention Study Group
Lancet Diabetes Endocrinol 2019 Jun;7(6):452-461. Epub 2019 Apr 26 doi: 10.1016/S2213-8587(19)30093-2. PMID: 31036503Free PMC Article
Huang Y, Cai X, Mai W, Li M, Hu Y
BMJ 2016 Nov 23;355:i5953. doi: 10.1136/bmj.i5953. PMID: 27881363Free PMC Article
Tuomilehto J, Lindström J, Eriksson JG, Valle TT, Hämäläinen H, Ilanne-Parikka P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas M, Salminen V, Uusitupa M; Finnish Diabetes Prevention Study Group
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Clinical prediction guides

Zhang B, Zhang X, Luo Z, Ren J, Yu X, Zhao H, Wang Y, Zhang W, Tian W, Wei X, Ding Q, Yang H, Jin Z, Tong X, Wang J, Zhao L
J Genet Genomics 2024 Jan;51(1):75-86. Epub 2023 Aug 29 doi: 10.1016/j.jgg.2023.08.005. PMID: 37652264
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Tsuchida K, Mitsuma W, Sato Y, Ozaki K, Soda S, Hatada K, Tanaka K, Hosaka Y, Imai S, Takahashi K, Matsubara T, Oda H
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Lillioja S
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Recent systematic reviews

Schlesinger S, Neuenschwander M, Barbaresko J, Lang A, Maalmi H, Rathmann W, Roden M, Herder C
Diabetologia 2022 Feb;65(2):275-285. Epub 2021 Oct 31 doi: 10.1007/s00125-021-05592-3. PMID: 34718834Free PMC Article
Vounzoulaki E, Khunti K, Abner SC, Tan BK, Davies MJ, Gillies CL
BMJ 2020 May 13;369:m1361. doi: 10.1136/bmj.m1361. PMID: 32404325Free PMC Article
Uusitupa M, Khan TA, Viguiliouk E, Kahleova H, Rivellese AA, Hermansen K, Pfeiffer A, Thanopoulou A, Salas-Salvadó J, Schwab U, Sievenpiper JL
Nutrients 2019 Nov 1;11(11) doi: 10.3390/nu11112611. PMID: 31683759Free PMC Article
Zafar MI, Mills KE, Zheng J, Regmi A, Hu SQ, Gou L, Chen LL
Am J Clin Nutr 2019 Oct 1;110(4):891-902. doi: 10.1093/ajcn/nqz149. PMID: 31374573
Huang Y, Cai X, Mai W, Li M, Hu Y
BMJ 2016 Nov 23;355:i5953. doi: 10.1136/bmj.i5953. PMID: 27881363Free PMC Article

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