U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

Abdominal obesity

MedGen UID:
90229
Concept ID:
C0311277
Finding
Synonyms: Abdominal Obesities; Abdominal Obesity; Central Obesities; Central Obesity; Obesities, Abdominal; Obesities, Central; Obesity, Abdominal; Obesity, Central
 
HPO: HP:0012743

Definition

Excessive fat around the stomach and abdomen. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVAbdominal obesity

Conditions with this feature

Prader-Willi syndrome
MedGen UID:
46057
Concept ID:
C0032897
Disease or Syndrome
Prader-Willi syndrome (PWS) is characterized by severe hypotonia and feeding difficulties in early infancy, followed in later infancy or early childhood by excessive eating and gradual development of morbid obesity (unless eating is externally controlled). Motor milestones and language development are delayed. All individuals have some degree of cognitive impairment. A distinctive behavioral phenotype (with temper tantrums, stubbornness, manipulative behavior, and obsessive-compulsive characteristics) is common. Hypogonadism is present in both males and females and manifests as genital hypoplasia, incomplete pubertal development, and, in most, infertility. Short stature is common (if not treated with growth hormone); characteristic facial features, strabismus, and scoliosis are often present.
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.
X-linked intellectual disability Cabezas type
MedGen UID:
337334
Concept ID:
C1845861
Disease or Syndrome
The Cabezas type of X-linked syndromic intellectual developmental disorder is characterized primarily by short stature, hypogonadism, and abnormal gait, with other more variable features such as speech delay, prominent lower lip, and tremor (Cabezas et al., 2000).
Abdominal obesity-metabolic syndrome quantitative trait locus 2
MedGen UID:
344224
Concept ID:
C1854170
Finding
Bardet-Biedl syndrome 1
MedGen UID:
422452
Concept ID:
C2936862
Disease or Syndrome
Bardet-Biedl syndrome is an autosomal recessive and genetically heterogeneous ciliopathy characterized by retinitis pigmentosa, obesity, kidney dysfunction, polydactyly, behavioral dysfunction, and hypogonadism (summary by Beales et al., 1999). Eight proteins implicated in the disorder assemble to form the BBSome, a stable complex involved in signaling receptor trafficking to and from cilia (summary by Scheidecker et al., 2014). Genetic Heterogeneity of Bardet-Biedl Syndrome BBS2 (615981) is caused by mutation in a gene on 16q13 (606151); BBS3 (600151), by mutation in the ARL6 gene on 3q11 (608845); BBS4 (615982), by mutation in a gene on 15q22 (600374); BBS5 (615983), by mutation in a gene on 2q31 (603650); BBS6 (605231), by mutation in the MKKS gene on 20p12 (604896); BBS7 (615984), by mutation in a gene on 4q27 (607590); BBS8 (615985), by mutation in the TTC8 gene on 14q32 (608132); BBS9 (615986), by mutation in a gene on 7p14 (607968); BBS10 (615987), by mutation in a gene on 12q21 (610148); BBS11 (615988), by mutation in the TRIM32 gene on 9q33 (602290); BBS12 (615989), by mutation in a gene on 4q27 (610683); BBS13 (615990), by mutation in the MKS1 gene (609883) on 17q23; BBS14 (615991), by mutation in the CEP290 gene (610142) on 12q21, BBS15 (615992), by mutation in the WDPCP gene (613580) on 2p15; BBS16 (615993), by mutation in the SDCCAG8 gene (613524) on 1q43; BBS17 (615994), by mutation in the LZTFL1 gene (606568) on 3p21; BBS18 (615995), by mutation in the BBIP1 gene (613605) on 10q25; BBS19 (615996), by mutation in the IFT27 gene (615870) on 22q12; BBS20 (619471), by mutation in the IFT172 gene (607386) on 9p21; BBS21 (617406), by mutation in the CFAP418 gene (614477) on 8q22; and BBS22 (617119), by mutation in the IFT74 gene (608040) on 9p21. The CCDC28B gene (610162) modifies the expression of BBS phenotypes in patients who have mutations in other genes. Mutations in MKS1, MKS3 (TMEM67; 609884), and C2ORF86 also modify the expression of BBS phenotypes in patients who have mutations in other genes. Although BBS had originally been thought to be a recessive disorder, Katsanis et al. (2001) demonstrated that clinical manifestation of some forms of Bardet-Biedl syndrome requires recessive mutations in 1 of the 6 loci plus an additional mutation in a second locus. While Katsanis et al. (2001) called this 'triallelic inheritance,' Burghes et al. (2001) suggested the term 'recessive inheritance with a modifier of penetrance.' Mykytyn et al. (2002) found no evidence of involvement of the common BBS1 mutation in triallelic inheritance. However, Fan et al. (2004) found heterozygosity in a mutation of the BBS3 gene (608845.0002) as an apparent modifier of the expression of homozygosity of the met390-to-arg mutation in the BBS1 gene (209901.0001). Allelic disorders include nonsyndromic forms of retinitis pigmentosa: RP51 (613464), caused by TTC8 mutation, and RP55 (613575), caused by ARL6 mutation.
Xq27.3q28 duplication syndrome
MedGen UID:
477152
Concept ID:
C3275521
Disease or Syndrome
Chromosome Xq27.3-q28 duplication syndrome is an X-linked recessive neurodevelopmental disorder characterized by mild mental retardation, mild facial dysmorphism, short stature, and primary testicular failure manifest as high-pitched voice, sparse body hair, abdominal obesity, and small testes. Female carriers may have short stature and premature ovarian failure (summary by Rio et al., 2010).
Abdominal obesity-metabolic syndrome 3
MedGen UID:
862798
Concept ID:
C4014361
Disease or Syndrome
Any metabolic syndrome in which the cause of the disease is a mutation in the DYRK1B gene.
ACTH-independent macronodular adrenal hyperplasia 2
MedGen UID:
863240
Concept ID:
C4014803
Disease or Syndrome
ACTH-independent macronodular adrenal hyperplasia-2 is an autosomal dominant tumor susceptibility with syndromic incomplete penetrance, as a second hit to the ARMC5 gene is required to develop macronodular hyperplasia (Assie et al., 2013).
LIPE-related familial partial lipodystrophy
MedGen UID:
863306
Concept ID:
C4014869
Disease or Syndrome
Familial partial lipodystrophy type 6 (FPLD6) is characterized by abnormal subcutaneous fat distribution, with variable excess accumulation of fat in the face, neck, shoulders, axillae, back, abdomen, and pubic region, and reduction in subcutaneous fat of the lower extremities. Progressive adult-onset myopathy is seen in some patients, and there is variable association with diabetes, hypertriglyceridemia, low high-density lipoprotein (HDL) cholesterol, and hepatic steatosis (Zolotov et al., 2017). For a general phenotypic description and a discussion of genetic heterogeneity of familial partial lipodystrophy (FPLD), see 151660.
Metabolic syndrome X
MedGen UID:
1640883
Concept ID:
C4552048
Disease or Syndrome
A clustering of abdominal obesity, high triglycerides, low levels of high density lipoprotein cholesterol (HDLC), high blood pressure, and elevated fasting glucose levels is sometimes called metabolic syndrome X (Reaven, 1988) or abdominal obesity-metabolic syndrome (Bjorntorp, 1991). The syndrome may affect nearly 1 in 4 U.S. adults and is considered a veritable epidemic (Ford et al., 2002). It is a major risk factor for both diabetes mellitus (see 125853 and Haffner et al., 1992) and cardiovascular disease (Isomaa et al., 2001). The etiology is complex, determined by the interplay of both genetic and environmental factors. The prevalence varies substantially among ethnic groups, with the highest rates in Mexican American women (Park et al., 2003). Other factors influencing the metabolic syndrome include age, smoking, alcohol, diet, and physical inactivity. Genetic Heterogeneity of Abdominal Obesity-Metabolic Syndrome AOMS2 (605572) has been mapped to chromosome 17p12. AOMS3 (615812) is caused by mutation in the DYRK1B gene (604556) on chromosome 19q13. AOMS4 (618620) is caused by mutation in the CELA2A gene (609443) on chromosome 1p36.
Isolated growth hormone deficiency, type 5
MedGen UID:
1648500
Concept ID:
C4748435
Disease or Syndrome
Combined pituitary hormone deficiency (CPHD) in man denotes impaired production of growth hormone (GH; 139250) and one or more of the other 5 anterior pituitary hormones. Some patients exhibit only GH deficiency, although approximately 50% of isolated GH deficiency progresses to CPHD (Gergics et al., 2021). Individuals with CPHD7 have been reported with isolated GH deficiency as well as combined deficiencies including thyroid-stimulating hormone (TSH; see 188540) and/or prolactin (PRL; 176760). In addition to severe postnatal short stature, patients exhibit delayed bone age and hypoplasia of the anterior pituitary, as well as distinctive facial dysmorphisms including frontal bossing and depressed nasal bridge (Argente et al., 2014; Verberne et al., 2020; Yamada et al., 2021). For general phenotypic information and a discussion of genetic heterogeneity of CPHD, see 613038.
Intellectual developmental disorder, X-linked, syndromic, Hackmann-Di Donato type
MedGen UID:
1716269
Concept ID:
C5393302
Disease or Syndrome
Hackmann-Di Donato-type X-linked syndromic intellectual developmental disorder (MRXSHD) is an X-linked recessive phenotype characterized by global developmental delay with hypotonia, delayed speech, and mildly delayed walking associated with somatic marfanoid features, including tall stature, long fingers, and mildly dysmorphic facies. Some patients may have cardiac defects, such as mitral valve regurgitation, as well as other anomalies related to connective tissue defects, such as scoliosis (summary by Fiordaliso et al., 2019).
Growth restriction, hypoplastic kidneys, alopecia, and distinctive facies
MedGen UID:
1784590
Concept ID:
C5543375
Disease or Syndrome
Growth restriction, hypoplastic kidneys, alopecia, and distinctive facies (GKAF) is characterized by microcephaly, congenital alopecia, distinctive craniofacial features, severe congenital sensorineural hearing loss, global developmental delay, hydrocephalus, hypoplastic kidneys with renal insufficiency, genital hypoplasia, and early mortality (Ito et al., 2018).

Professional guidelines

PubMed

Kumar S, Mittal A, Babu D, Mittal A
Curr Diabetes Rev 2021;17(4):437-456. doi: 10.2174/1573399816666201103143225. PMID: 33143632
Weihe P, Weihrauch-Blüher S
Curr Obes Rep 2019 Dec;8(4):472-479. doi: 10.1007/s13679-019-00357-x. PMID: 31691175
Farshchi H, Rane A, Love A, Kennedy RL
J Obstet Gynaecol 2007 Nov;27(8):762-73. doi: 10.1080/01443610701667338. PMID: 18097891

Recent clinical studies

Etiology

Zhu X, Ding L, Zhang X, Xiong Z
J Affect Disord 2023 Nov 1;340:523-528. Epub 2023 Aug 16 doi: 10.1016/j.jad.2023.08.067. PMID: 37595895
Qiao T, Luo T, Pei H, Yimingniyazi B, Aili D, Aimudula A, Zhao H, Zhang H, Dai J, Wang D
Cardiovasc Diabetol 2022 Nov 1;21(1):225. doi: 10.1186/s12933-022-01670-x. PMID: 36320060Free PMC Article
Jayawardena R, Sooriyaarachchi P, Misra A
Expert Rev Endocrinol Metab 2021 Nov;16(6):339-349. Epub 2021 Sep 29 doi: 10.1080/17446651.2021.1982381. PMID: 34586004
Yuan S, Bruzelius M, Xiong Y, Håkansson N, Åkesson A, Larsson SC
J Thromb Haemost 2021 Feb;19(2):460-469. Epub 2020 Dec 8 doi: 10.1111/jth.15168. PMID: 33179380Free PMC Article
Dong Y, Zhou J, Zhu Y, Luo L, He T, Hu H, Liu H, Zhang Y, Luo D, Xu S, Xu L, Liu J, Zhang J, Teng Z
Biosci Rep 2017 Dec 22;37(6) Epub 2017 Dec 12 doi: 10.1042/BSR20170945. PMID: 29026008Free PMC Article

Diagnosis

Sandsdal RM, Juhl CR, Jensen SBK, Lundgren JR, Janus C, Blond MB, Rosenkilde M, Bogh AF, Gliemann L, Jensen JB, Antoniades C, Stallknecht BM, Holst JJ, Madsbad S, Torekov SS
Cardiovasc Diabetol 2023 Feb 25;22(1):41. doi: 10.1186/s12933-023-01765-z. PMID: 36841762Free PMC Article
Wan H, Wang Y, Xiang Q, Fang S, Chen Y, Chen C, Zhang W, Zhang H, Xia F, Wang N, Lu Y
Cardiovasc Diabetol 2020 Jul 31;19(1):118. doi: 10.1186/s12933-020-01095-4. PMID: 32736628Free PMC Article
Ojeda-Rodríguez A, Zazpe I, Morell-Azanza L, Chueca MJ, Azcona-Sanjulian MC, Marti A
Nutrients 2018 Oct 13;10(10) doi: 10.3390/nu10101500. PMID: 30322156Free PMC Article
Fang H, Berg E, Cheng X, Shen W
Curr Opin Clin Nutr Metab Care 2018 Sep;21(5):360-365. doi: 10.1097/MCO.0000000000000485. PMID: 29916924Free PMC Article
Després JP, Lemieux I
Nature 2006 Dec 14;444(7121):881-7. doi: 10.1038/nature05488. PMID: 17167477

Therapy

Sandsdal RM, Juhl CR, Jensen SBK, Lundgren JR, Janus C, Blond MB, Rosenkilde M, Bogh AF, Gliemann L, Jensen JB, Antoniades C, Stallknecht BM, Holst JJ, Madsbad S, Torekov SS
Cardiovasc Diabetol 2023 Feb 25;22(1):41. doi: 10.1186/s12933-023-01765-z. PMID: 36841762Free PMC Article
Yuan L, Chang M, Wang J
Age Ageing 2021 Jun 28;50(4):1118-1128. doi: 10.1093/ageing/afab039. PMID: 33693472
Ojeda-Rodríguez A, Zazpe I, Morell-Azanza L, Chueca MJ, Azcona-Sanjulian MC, Marti A
Nutrients 2018 Oct 13;10(10) doi: 10.3390/nu10101500. PMID: 30322156Free PMC Article
Geiker NRW, Astrup A, Hjorth MF, Sjödin A, Pijls L, Markus CR
Obes Rev 2018 Jan;19(1):81-97. Epub 2017 Aug 28 doi: 10.1111/obr.12603. PMID: 28849612
Chen IJ, Liu CY, Chiu JP, Hsu CH
Clin Nutr 2016 Jun;35(3):592-9. Epub 2015 May 29 doi: 10.1016/j.clnu.2015.05.003. PMID: 26093535

Prognosis

Mambrini SP, Menichetti F, Ravella S, Pellizzari M, De Amicis R, Foppiani A, Battezzati A, Bertoli S, Leone A
Nutrients 2023 May 31;15(11) doi: 10.3390/nu15112583. PMID: 37299546Free PMC Article
Liu M, Zhang Z, Zhou C, Ye Z, He P, Zhang Y, Li H, Liu C, Qin X
J Cachexia Sarcopenia Muscle 2022 Apr;13(2):1064-1075. Epub 2022 Jan 23 doi: 10.1002/jcsm.12921. PMID: 35068076Free PMC Article
Saklayen MG
Curr Hypertens Rep 2018 Feb 26;20(2):12. doi: 10.1007/s11906-018-0812-z. PMID: 29480368Free PMC Article
Chang P, Friedenberg F
Gastroenterol Clin North Am 2014 Mar;43(1):161-73. Epub 2013 Dec 27 doi: 10.1016/j.gtc.2013.11.009. PMID: 24503366Free PMC Article
Bardou M, Barkun AN, Martel M
Gut 2013 Jun;62(6):933-47. Epub 2013 Mar 12 doi: 10.1136/gutjnl-2013-304701. PMID: 23481261

Clinical prediction guides

Jurczewska J, Ostrowska J, Chełchowska M, Panczyk M, Rudnicka E, Kucharski M, Smolarczyk R, Szostak-Węgierek D
Nutrients 2023 Aug 20;15(16) doi: 10.3390/nu15163652. PMID: 37630842Free PMC Article
West HW, Siddique M, Williams MC, Volpe L, Desai R, Lyasheva M, Thomas S, Dangas K, Kotanidis CP, Tomlins P, Mahon C, Kardos A, Adlam D, Graby J, Rodrigues JCL, Shirodaria C, Deanfield J, Mehta NN, Neubauer S, Channon KM, Desai MY, Nicol ED, Newby DE, Antoniades C; ORFAN Investigators
JACC Cardiovasc Imaging 2023 Jun;16(6):800-816. Epub 2023 Feb 8 doi: 10.1016/j.jcmg.2022.11.018. PMID: 36881425Free PMC Article
Wan H, Wang Y, Xiang Q, Fang S, Chen Y, Chen C, Zhang W, Zhang H, Xia F, Wang N, Lu Y
Cardiovasc Diabetol 2020 Jul 31;19(1):118. doi: 10.1186/s12933-020-01095-4. PMID: 32736628Free PMC Article
Ojeda-Rodríguez A, Zazpe I, Morell-Azanza L, Chueca MJ, Azcona-Sanjulian MC, Marti A
Nutrients 2018 Oct 13;10(10) doi: 10.3390/nu10101500. PMID: 30322156Free PMC Article
Chan DS, Norat T
Curr Treat Options Oncol 2015 May;16(5):22. doi: 10.1007/s11864-015-0341-9. PMID: 25904412

Recent systematic reviews

Silveira EA, Mendonça CR, Delpino FM, Elias Souza GV, Pereira de Souza Rosa L, de Oliveira C, Noll M
Clin Nutr ESPEN 2022 Aug;50:63-73. Epub 2022 Jun 14 doi: 10.1016/j.clnesp.2022.06.001. PMID: 35871953
Lane MM, Davis JA, Beattie S, Gómez-Donoso C, Loughman A, O'Neil A, Jacka F, Berk M, Page R, Marx W, Rocks T
Obes Rev 2021 Mar;22(3):e13146. Epub 2020 Nov 9 doi: 10.1111/obr.13146. PMID: 33167080
Ma X, Chen Q, Pu Y, Guo M, Jiang Z, Huang W, Long Y, Xu Y
Obes Res Clin Pract 2020 Jan-Feb;14(1):1-8. Epub 2020 Jan 7 doi: 10.1016/j.orcp.2019.12.002. PMID: 31918985
Ahirwar R, Mondal PR
Diabetes Metab Syndr 2019 Jan-Feb;13(1):318-321. Epub 2018 Sep 21 doi: 10.1016/j.dsx.2018.08.032. PMID: 30641719
Carbone A, Al Salhi Y, Tasca A, Palleschi G, Fuschi A, De Nunzio C, Bozzini G, Mazzaferro S, Pastore AL
Minerva Urol Nefrol 2018 Aug;70(4):393-400. Epub 2018 May 31 doi: 10.23736/S0393-2249.18.03113-2. PMID: 29856171

Supplemental Content

Table of contents

    Clinical resources

    Practice guidelines

    • PubMed
      See practice and clinical guidelines in PubMed. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.
    • Bookshelf
      See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Consumer resources

    Recent activity

    Your browsing activity is empty.

    Activity recording is turned off.

    Turn recording back on

    See more...