Endocrine function in human obesity

Glass, Allan R.; Burman, Kenneth D.; Dahms, William T.; Boehm, Timothy M.

doi:10.1016/0026-0495(81)90224-9

Cited by 247 publications

(93 citation statements)

References 201 publications

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“…It is known that in man, obesity results in impaired GH release, which is restored when the obesity is corrected (48). However, it is unlikely that the GH suppression observed in the present study is secondary to the obesity, since similar suppression has been reported in nonobese, VMH-lesioned animals (10).…”

Section: Discussioncontrasting

confidence: 36%

Effects of Obesity-Inducing Ventromedial Hypothalamic Lesions on Pulsatile Growth Hormone and Insulin Secretion: Evidence for the Existence of a Growth Hormone-Releasing Factor*

Eikelboom

Tannenbaum

1983

Endocrinology

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Section: Discussioncontrasting

confidence: 36%

Effects of Obesity-Inducing Ventromedial Hypothalamic Lesions on Pulsatile Growth Hormone and Insulin Secretion: Evidence for the Existence of a Growth Hormone-Releasing Factor*

Eikelboom

Tannenbaum

1983

Endocrinology

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“…The decrease in ovarian cancer risk with increasing BMI observed in our data is consistent with this hypothesis, because excessive body weight and obesity, have been associated with an increased number of anovulatory cycles, as well as with anovulation. 27,28 The relationship of obesity with ovarian cancer under the gonadotropin hypothesis is more complex. This hypothesis states that excessive gonadotropin stimulation, directly or indirectly through stimulation of the ovarian steroidogenic activity, results in increased proliferation and malignant transformation of the ovarian epithelium trapped within inclusion cysts formed through repeated invaginations of the epithelium during ovulation.…”

Section: Discussionmentioning

confidence: 99%

Body mass index in relation to ovarian cancer: A multi‐centre nested case‐control study

Lukanova

Toniolo

Lundin

et al. 2002

Intl Journal of Cancer

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The incidence of ovarian cancer is up to 10 times higher in Western countries than in rural Asia and Africa. One common consequence of a Western lifestyle is the development of excessive body weight and obesity. A multi-centre prospective study was conducted to investigate the association between body mass index (BMI) and ovarian cancer risk. A case-control study was nested within 3 prospective cohorts in New York (USA), Umeå (Sweden) and Milan (Italy). Information on anthropometry, demographic characteristics, medical history and lifestyle was obtained at the time of subjects' recruitment in each cohort. Women diagnosed with primary, invasive epithelial ovarian cancer from the 3 cohorts (n ‫؍‬ 122) diagnosed 12 months or later after recruitment into the respective cohort served as case subjects. For each case subject, 2 control subjects that matched the case subject on cohort, menopausal status, age and date of recruitment were randomly identified. Data were analyzed by conditional logistic regression. There was an inverse association between BMI and ovarian cancer risk. Key words: body mass index; height; anthropometry; ovarian cancer; prospective study; cohort Age-standardised incidence rates of ovarian cancer are up to 10 times higher in Western, industrialized countries than in rural Africa or Asia. 1 Migration studies have shown that women of Chinese and Japanese descent who reside in the U.S. tend to have higher incidence rates than their Asian counterparts and that in women 20 -49 years of age, the incidence of ovarian cancer is similar in U.S.-born Chinese women and U.S. white women. 2 These observations suggest that environmental factors related to a Western lifestyle may be associated with the increase in ovarian cancer risk. A common consequence of Western lifestyle, which has been shown to increase risk of some female cancers, such as postmenopausal breast and endometrial cancers, is the development of excessive body weight and obesity. Increase in body weight relative to body height, as reflected by an increased body mass index (BMI), may alter cancer risk through changes in endogenous hormone metabolism. [3][4][5] The role of a greater body weight is considerably clearer in relation to breast and endometrial cancers than to ovarian cancer, for which the majority of studies report non-significant associations. 5-8 A recent extensive review, including 29 reports on the association of body weight/BMI with ovarian cancer risk, concluded that there is a direct, however weak, association of increased BMI with ovarian cancer based on the results of cohort [summary OR 1.2 (1.1-1.3)] and populationbased case-control studies [summary OR 1.4 (1.2-1.6)]. 9 Hospitalbased case-control studies showed heterogeneous results; however, some of the differences in the results might reflect specific characteristics of the control groups included, e.g., a higher proportion of overweight women in the control series due to obesity-related conditions such as cardiovascular disease and diabetes. 9 In this paper, we report t...

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“…We concluded that FT levels are dependent on the degree of obesity, massively obese men (BMI ³ 35.1kg/m 2 ) being considered as candidates for consistently low FT levels. Além disso, também foi observado por diversos pesquisadores, decréscimo na capacidade de ligação da globulina carregadora de hormônios sexuais (SHBG) em homens obesos comparativamente à população masculina de peso normal e dentro da mesma faixa et·ria (1)(2)(3)(4)(6)(7)(8).…”

Section: Introductionunclassified

A função gonadal do homem obeso

Lima

Cavaliere

Halpern

et al. 2000

Arq Bras Endocrinol Metab

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RESUMOEm homens obesos, os níveis séricos de globulina ligadora de hormônios sexuais (GLHS), bem como de testosterona total, (TT) estão diminuídos. Dados relativos aos níveis séricos de testosterona livre (TL) são controversos. Homens com obesidade mórbida apresentam valores plasmáticos de testosterona livre diminuídos, levando à alteração dos mecanismos de retro-regulação. O decréscimo funcional da amplitude do pulso de LH, bem como a diminuição dos níveis de LH, seriam a causa do hipoandrogenismo. Estudamos dois grupos de homens obesos: Grupo 1 (IMC £ 35kg/m 2 ) e Grupo 2 (IMC ³ 35kg/m 2 ) antes e após seis meses de dieta hipocalórica (1.200Kcal/dia). Todos os pacientes utilizaram dexfenfluramina (15mg 2x ao dia) durante todo o período do estudo. Níveis plasmáticos de insulina, bem como valores séricos de testosterona total, testosterona livre e LH foram dosados antes e após a perda de peso. Pacientes com obesidade moderada (IMC = 32,3 ± 1,9kg/m 2 ) apresentaram diminuição significativa na concentração sérica de TT (390 ± 120ng/dL), bem como de TL (média ± DP 16,0 ± 4,8pg/mL) quando comparados a normais. A concentração de LH sérico (4,5 ± 2,9mlU/mL) foi considerada normal. Níveis de insulina mostravam-se elevados em todos os pacientes (46,3 ± 30,1mU/mL). Após a perda de peso, notou-se aumento significante (p < 0,01) dos níveis séricos de LH, TT e TL concomitante à queda da concentração de insulina plasmática. Em homens com obesidade de grande porte (IMC = 43,0 ± 6,7kg/m 2 ), os níveis de TT (320 ± 110ng/dL), TL (11,0 ± 2,1pg/mL) e LH (3,1 ±1,3mlU/mL) mostraram-se significativamente menores quando comparados ao Grupo 1 e aos controles normais. Como esperado, após a perda de peso, os níveis séricos de TT, TL e LH aumentaram significativamente enquanto a concentração plasmática de insulina diminuiu. Concluímos que os níveis de TL são dependentes do grau de obesidade: homens com obesidade de grande porte (IMC ³ 35kg/m 2 ) são considerados como candidatos a apresentarem baixos valores séricos de TL. Unitermos: Testosterona; Hipogonadismo; Obesidade; Perda de peso; Insulina; Gonadostato ABSTRACTIn obese men, sex hormone-binding globulin (SHBG) as well as total testosterone (TT) levels are decreased. Data concerning serum free testosterone (FT) levels in obese men are discordant. FT levels are decreased in only some morbidly obese men consistent with an impairment of the feedback regulatory mechanism. It has been suggested that a functional decrease of LH pulse amplitude and serum LH levels are reflected in their hypoandrogenism. We have studied two groups of obese men (Group 1: BMI £ 35kg/m 2 and Group 2: BMI ³ 35.1kg/m 2 ) before and after six months of a low calorie diet (1200kcal/day), Every patient received a therapeutic prescription of

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Endocrine function in human obesity

Cited by 247 publications

References 201 publications

Effects of Obesity-Inducing Ventromedial Hypothalamic Lesions on Pulsatile Growth Hormone and Insulin Secretion: Evidence for the Existence of a Growth Hormone-Releasing Factor*

Effects of Obesity-Inducing Ventromedial Hypothalamic Lesions on Pulsatile Growth Hormone and Insulin Secretion: Evidence for the Existence of a Growth Hormone-Releasing Factor*

Body mass index in relation to ovarian cancer: A multi‐centre nested case‐control study

A função gonadal do homem obeso

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