Body mass index and ovarian function are associated with endocrine and metabolic abnormalities in women with hyperandrogenic syndrome

2008 ◽  
Vol 158 (5) ◽  
pp. 711-719 ◽  
Author(s):  
S Cupisti ◽  
N Kajaia ◽  
R Dittrich ◽  
H Duezenli ◽  
M W Beckmann ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Density Lipoprotein ◽  
Sex Hormone Binding Globulin ◽  
Oral Glucose ◽  
Sensitivity Index ◽  
Metabolic Abnormalities ◽  
Insulin Levels ◽  
Homeostatic Model

BackgroundThe aim of this study was to evaluate associations of clinical features, such as hirsutism, polycystic ovaries (PCOs), ovulatory dysfunction, and body mass index (BMI) ≥25 kg/m2, with metabolic abnormalities in hyperandrogenic women.MethodsHirsutism was based on the modified Ferriman–Gallwey score. Ovulatory function was classified as eumenorrhea, oligomenorrhea and amenorrhea, and PCOs were assessed using the ultrasound criteria recommended in the Rotterdam definition. An oral glucose tolerance test was performed. Different insulin resistance (IR) indices were calculated.ResultsHirsute women had significantly higher BMI, DHEA sulfate (DHEAS) and free androgen index (FAI), and significantly lower values for sex hormone-binding globulin (SHBG). Women with amenorrhea were younger in comparison to women with eumenorrhea and had significantly higher values for fasting insulin (FI) and 1- and 2-h insulin levels; lower values for glucose to insulin ratio (GIR), quantitative insulin sensitivity check index (QUICKI), and SHBG. Women with PCO had significantly higher levels of LH and low-density lipoprotein (LDL), whereas high-density lipoprotein (HDL) levels were significantly lower. Women with a BMI ≥25 kg/m2 had significantly higher values for age, fasting plasma glucose, FI, and 1- and 2-h glucose and insulin levels, homeostatic model for assessment of IR (HOMA-IR), homeostatic model for assessment of B-cell function (HOMA-B), and FAI, whereas their GIR, insulin sensitivity index, QUICKI, SHBG, and HDL were significantly lower.ConclusionsIn women with hyperandrogenic syndrome, BMI≥25 kg/m2 and amenorrhea appear to be associated with severe endocrine and metabolic abnormalities.

scholarly journals The Metabolic Phenotype of Prader-Willi Syndrome (PWS) in Childhood: Heightened Insulin Sensitivity Relative to Body Mass Index

2011 ◽  
Vol 96 (1) ◽  
pp. E225-E232 ◽  
Author(s):  
Andrea M. Haqq ◽  
Michael J. Muehlbauer ◽  
Christopher B. Newgard ◽  
Steven Grambow ◽  
Michael Freemark
Keyword(s):  
Body Mass Index ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Density Lipoprotein ◽  
High Sensitivity ◽  
Metabolic Phenotype ◽  
Prader Willi Syndrome ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Total Adiponectin

Context: Insulin sensitivity is higher in patients with Prader-Willi syndrome (PWS) than in body mass index-matched obese controls (OCs). Factors contributing to the heightened insulin sensitivity of PWS remain obscure. We compared the fasting levels of various hormones, cytokines, lipids, and liver function tests in 14 PWS patients and 14 OCs with those in 14 age- and gender-matched lean children (LC). We hypothesized that metabolic profiles of children with PWS are comparable with those of LC, but different from those of OCs. Results: Leptin levels were comparable in PWS patients and OCs, suggesting comparable degrees of adiposity. Glucose levels were comparable among groups. However, fasting insulin concentrations and homeostasis model assessment insulin resistance index were lower in PWS patients than in OCs (P < 0.05) and similar to LC. Moreover, high-density lipoprotein levels were lower and triglycerides higher in OCs (P < 0.05) but not PWS patients. Total adiponectin, high-molecular-weight (HMW) adiponectin and the HMW to total adiponectin ratio were higher in PWS patients (P < 0.05) than in OCs and similar to LC. High-sensitivity C-reactive protein and IL-6 levels were higher in OCs than in PWS patients or LC (P < 0.05). Nevertheless, PAI-1 levels were elevated in both OC and PWS patients. There were no group differences in glucagon-like peptide-1, macrophage chemoattractant protein-1, TNFα, IL-2, IL-8, IL-10, IL-12p40, IL-18, resistin, total or low-density lipoprotein cholesterol, aspartate aminotransferase, or alanine aminotransferase. Conclusions: The heightened insulin sensitivity of PWS patients relative to OCs is associated with higher levels of adiponectin and lower levels of high-sensitivity C-reactive protein and IL-6. Future studies will determine whether PWS children are protected from obesity comorbidities such as type 2 diabetes, hyperlipidemia, and nonalcoholic fatty liver disease.

Analysis of candidate genes in Polish families with obesity

2004 ◽  
Vol 42 (5) ◽  
Author(s):  
Malgorzata Malczewska-Malec ◽  
Iwona Wybranska ◽  
Iwona Leszczynska-Golabek ◽  
Lukasz Partyka ◽  
Jadwiga Hartwich ◽  
...  
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Tolerance Test ◽  
Whole Body ◽  
Oral Glucose ◽  
Sensitivity Index ◽  
Model Assessment ◽  
The Metabolic Syndrome

AbstractThis study analyzes the relationship between risk factors related to overweight/obesity, insulin resistance, lipid tolerance, hypertension, endothelial function and genetic polymorphisms associated with: i) appetite regulation (leptin, melanocortin-3-receptor (MCR-3), dopamine receptor 2 (D2R)); ii) adipocyte differentiation and insulin sensitivity (peroxisome proliferator-activated receptor-γThe 122 members of 40 obese Caucasian families from southern Poland participated in the study. The genotypes were analyzed by restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) or by direct sequencing. Phenotypes related to obesity (body mass index (BMI), fat/lean body mass composition, waist-to-hip ratio (WHR)), fasting lipids, glucose, leptin and insulin, as well as insulin during oral glucose tolerance test (OGTT) (4 points within 2 hours) and during oral lipid tolerance test (OLTT) (5 points within 8 hours) were assessed. The insulin sensitivity indexes: homeostasis model assessment of insulin resistance, whole body insulin sensitivity index, hepatic insulin sensitivity and early secretory response to an oral glucose load (HOMA-IR, ISI-COMP, ISI-HOMA and DELTA) were calculated.The single gene mutations such as CWe conclude that the polymorphisms we investigated were weakly correlated with obesity but significantly modified the risk factors of the metabolic syndrome.

scholarly journals Impaired Insulin Secretion in the Turner Metabolic Syndrome

2004 ◽  
Vol 89 (7) ◽  
pp. 3516-3520 ◽  
Author(s):  
Vladimir K. Bakalov ◽  
Margaret M. Cooley ◽  
Michael J. Quon ◽  
Mei Lin Luo ◽  
Jack A. Yanovski ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Body Mass Index ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Cell Function ◽  
Insulin Response ◽  
Area Under The Curve ◽  
Oral Glucose ◽  
Glucose Challenge

Abstract An increased prevalence of impaired glucose homeostasis (IGH) and diabetes mellitus is reported in monosomy X, or Turner syndrome (TS). To determine whether IGH is an intrinsic feature of this syndrome, independent of obesity or hypogonadism, we compared results of a standard oral glucose challenge in age- and body mass index-matched women with TS and with karyotypically normal premature ovarian failure (POF). Fasting glucose levels were normal in both groups, but glucose values after oral glucose challenge were higher in TS [2-h glucose, 135 ± 36 mg/dl (7.5 ± 2.0 mmol/liter) in TS and 97 ± 18 mg/dl (5.4 ± 1.0 mmol/liter) in POF; P < 0.0001]. Glucose-stimulated insulin secretion was lower in TS; e.g. the initial insulin response (ΔI/ΔG30) was decreased by 60% compared with POF (P < 0.0001). We also compared responses to a standard iv glucose tolerance test in women with TS and in age- and body mass index-matched normal women and found that the insulin area under the curve was 50% lower in women with TS (P = 0.003). Insulin sensitivity measured by the quantitative insulin sensitivity check index was higher in women with TS compared with both control groups. Thus, IGH is not secondary to obesity or hypogonadism in TS, but it is a distinct entity characterized by decreased insulin secretion, suggesting that haploinsufficiency for X-chromosome gene(s) impairs β-cell function and predisposes to diabetes mellitus in TS.

Effects of age and anesthetic on plasma glucose and insulin levels and insulin sensitivity in spontaneously hypertensive and Wistar rats

2002 ◽  
Vol 80 (10) ◽  
pp. 962-970 ◽  
Author(s):  
Erika R Vera ◽  
Mary L Battell ◽  
Sanjay Bhanot ◽  
John H McNeill
Keyword(s):  
Body Weight ◽  
Insulin Sensitivity ◽  
Wistar Rats ◽  
Oral Glucose ◽  
Sensitivity Index ◽  
Insulin Sensitivity Index ◽  
Spontaneously Hypertensive ◽  
Insulin Levels ◽  
Insulin Resistant ◽  
Glucose Tolerance Tests

We examined the effects of anesthetic, age, and strain on oral glucose tolerance tests (OGTT, 1 g/kg body weight) and intraperitoneal glucose tolerance tests (IPGTT, 2 g/kg body weight) in spontaneously hypertensive (SH) and Wistar rats. Pentobarbital anesthesia caused an elevation in basal glucose and insulin levels in Wistar rats at 9 and 16 weeks of age and in SH rats at 9 weeks. Anesthesia increased the insulin output during an OGTT in both strains of rats while glucose was unchanged. Anesthesia reduced the insulin sensitivity index calculated from the OGTT but not from the IPGTT data. The age of the rats (9–11 vs. 16–18 weeks) had no effect on the basal glucose or insulin levels, but older Wistar rats had a greater insulin output following oral glucose and older SH rats had a greater insulin output following intraperitoneal glucose. On the basis of the insulin sensitivity index, SH rats were clearly more insulin resistant than age-matched Wistar rats. The SH rats also had higher basal insulin levels, as well as higher insulin output, following both glucose challenges. In summary, SH rats are more insulin resistant than Wistar rats, and anesthesia, which elevated basal glucose and insulin levels and increased the insulin output in response to a glucose challenge, may increase insulin resistance.Key words: spontaneously hypertensive rats, insulin sensitivity index, anesthesia, age.

scholarly journals Relation among Left Ventricular Mass, Insulin Resistance, and Blood Pressure in Nonobese Subjects1

1998 ◽  
Vol 83 (12) ◽  
pp. 4284-4288
Author(s):  
Robert A. Phillips ◽  
Lawrence R. Krakoff ◽  
Andrea Dunaif ◽  
Diane T. Finegood ◽  
Richard Gorlin ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Body Mass Index ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Tolerance Test ◽  
Left Ventricular ◽  
Sensitivity Index ◽  
Consecutive Series ◽  
Arterial Blood

Because left ventricular (LV) mass (LVM) is a powerful predictor of future cardiovascular events, it is important to identify hemodynamic and nonhemodynamic factors that increase LVM. We studied the separate contribution to LVM of daily arterial blood pressure (BP) and insulin resistance in a consecutive series of 29 (mean ± sd age, 43 ± 13 yr) nonobese (body mass index, 24 ± 1.8 kg/m2), nondiabetic, glucose-tolerant subjects with untreated borderline or mild hypertension. The insulin sensitivity index (SI) was quantitatively determined from the frequently sampled iv glucose tolerance test. BP was characterized by ambulatory 24-h BP monitoring, and LVM index (LVMI) was determined by two-dimensional directed M-mode echocardiography. LVMI was directly related to 24-h mean BP (r = 0.47; P = 0.01). LMVI was also significantly related to SI (r = −0.43; P = 0.02). In this nonobese group, neither LVMI nor SI was related to body mass index or age. After adjustment for the influence of BP on LVMI, a significant relation remained between LVMI and SI (P < 0.05). We conclude that in nonobese subjects with high normal BP, insulin sensitivity is related to LVM independently of BP and may be an important modulator of LV growth. In addition to a reduction of arterial BP, optimal prevention of LV hypertrophy in hypertensives may require improved insulin sensitivity.

Relationship of high density lipoprotein cholesterol with total and free testosterone and sex hormone binding globulin

1983 ◽  
Vol 104 (2) ◽  
pp. 253-256 ◽  
Author(s):  
R. F. Heller ◽  
M. J. Wheeler ◽  
J. Micallef ◽  
N. E. Miller ◽  
B. Lewis
Keyword(s):  
Body Mass Index ◽  
High Density Lipoprotein ◽  
Body Mass ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Free Testosterone ◽  
Sex Hormone ◽  
Sex Hormone Binding Globulin ◽  
Total Testosterone ◽  
Hormone Binding

Abstract. A cross-sectional study was performed to see if the previously described association between high density lipoprotein (HDL) cholesterol and plasma total testosterone concentration reflected a relationship with free testosterone or with sex hormone binding globulin (SHBG). In 295 employed middle-aged men, measurements were made of total testosterone and SHBG in serum and of testosterone in saliva, and also of plasma total and HDL cholesterol, plasma triglycerides and other factors which might influence HDL cholesterol levels such as body mass index, alcohol and smoking habits and thyroid hormone levels. In a multiple regression analysis using the GLIM package programme total testosterone concentrations had a persistent positive association with HDL cholesterol (t = 3.5, P < 0.001) – this association was independent of SHBG (which had a negative association with HDL: t = −1.8, P <0.07. The association of HDL cholesterol with testosterone was independent of and stronger than the association of HDL cholesterol with body mass index, alcohol intake and cigarette smoking. Salivary testosterone (a measure of the circulating free hormone) also had a positive independent association with HDL cholesterol. The relationship between HDL cholesterol and testosterone thus appears to reflect an association with circulating hormone levels rather than with the hormone binding globulin.

scholarly journals The influence of obesity in patients with prostate cancer - Review of the literature

2013 ◽  
Vol 3 (4) ◽  
pp. 80 ◽  
Author(s):  
Maximilien C. Goris Gbenou
Keyword(s):  
Prostate Cancer ◽  
Body Mass Index ◽  
Risk Factor ◽  
Body Mass ◽  
Functional Foods ◽  
Specific Antigen ◽  
Density Lipoprotein ◽  
Cancer Control ◽  
Sex Hormone Binding Globulin ◽  
Increased Risk

Recent studies have demonstrated an association between higher body mass index and increased aggressiveness in prostate cancer. The present narrative review, based on a search of Medline® and Embase® databases from October 1982 to October 2012, explores the relationship between higher body mass index and localized prostate cancer. In particular, the current epidemiological and mechanistic evidence for interactions between obesity and prostate cancer are discussed. Obesity is associated with alterations in androgen levels, decreased sex hormone binding globulin and increased estrogen levels, insulin resistance, hyperglycemia, alterations in plasma lipoprotein levels particularly raised triglycerides and reduced high density lipoprotein, decreased levels of adiponectin, and increased levels of circulating insulin-growth factor- 1, leptin and dietary saturated fats. Obese men have more aggressive prostate cancer with a greater percentage prostate involvement, increased tumor volume and higher-grade disease, enlarged prostates, high prostate-specific antigen levels, increased risk of having positive margins and recurrence. Moreover, there is strong evidence of the beneficial effects of functional foods for the treatment of obesity. Additionally, an increasing number of studies support that obesity-induced inflammation plays an important role in the development of obesity-related pathologies. Despite, the beneficial role of nutriment in prostate cancer control, the use of functional foods in prostate cancer is not recommended for lack of large epidemiological studies. This data supports the hypothesis that obese men have more aggressive prostate cancers and that the obesity is a modifiable risk factor of prostate cancer. Key Words: prostate cancer, metabolic syndrome, obesity, high BMI, risk factor, diet, functional foods.

scholarly journals The Metabolic Phenotype of Prader-Willi Syndrome (PWS) in Childhood: Heightened Insulin Sensitivity Relative to Body Mass Index

2010 ◽  
Vol 31 (6) ◽  
pp. 943-943
Author(s):  
Andrea M. Haqq ◽  
Michael J. Muehlbauer ◽  
Christopher B. Newgard ◽  
Steven Grambow ◽  
Michael Freemark
Keyword(s):  
Body Mass Index ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Density Lipoprotein ◽  
High Sensitivity ◽  
Metabolic Phenotype ◽  
Prader Willi Syndrome ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Total Adiponectin

Context Insulin sensitivity is higher in patients with Prader-Willi syndrome (PWS) than in body mass index-matched obese controls (OCs). Factors contributing to the heightened insulin sensitivity of PWS remain obscure. We compared the fasting levels of various hormones, cytokines, lipids, and liver function tests in 14 PWS patients and 14 OCs with those in 14 age- and gender-matched lean children (LC). We hypothesized that metabolic profiles of children with PWS are comparable with those of LC but different from those of OCs. Results Leptin levels were comparable in PWS patients and OCs, suggesting comparable degrees of adiposity. Glucose levels were comparable among groups. However, fasting insulin concentrations and homeostasis model assessment insulin resistance index were lower in PWS patients than in OCs (P &lt; 0.05) and similar to LC. Moreover, high-density lipoprotein levels were lower and triglycerides higher in OCs (P &lt; 0.05) but not PWS patients. Total adiponectin, high-molecular-weight (HMW) adiponectin and the HMW to total adiponectin ratio were higher in PWS patients (P &lt; 0.05) than in OCs and similar to LC. High-sensitivity C-reactive protein and IL-6 levels were higher in OCs than in PWS patients or LC (P &lt; 0.05). Nevertheless, PAI-1 levels were elevated in both OC and PWS patients. There were no group differences in glucagon-like peptide-1-(7-36)-amide, macrophage chemoattractant protein-1, TNFα, IL-2, IL-8, IL-10, IL-12p40, IL-18, resistin, total or low-density lipoprotein cholesterol, aspartate aminotransferase, or aminotransferase. Conclusions The heightened insulin sensitivity of PWS patients relative to OCs is associated with higher levels of adiponectin and lower levels of high-sensitivity C-reactive protein and IL-6. Future studies will determine whether PWS children are protected from obesity comorbidities such as type 2 diabetes, hyperlipidemia, and nonalcoholic fatty liver disease.

scholarly journals Association of Inflammation Markers with Impaired Insulin Sensitivity and Coagulative Activation in Obese Healthy Women

2003 ◽  
Vol 88 (11) ◽  
pp. 5321-5326 ◽  
Author(s):  
Mario Romano ◽  
Maria Teresa Guagnano ◽  
Giovanni Pacini ◽  
Sergio Vigneri ◽  
Angela Falco ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Mass Index ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Factor Viia ◽  
Sensitivity Index ◽  
Insulin Sensitivity Index ◽  
Impaired Insulin ◽  
Tgf Β1 ◽  
Pai 1

Abstract Insulin resistance is associated with a low chronic inflammatory state. In this study we investigated the relationship between impaired insulin sensitivity and selected markers of inflammation and thrombin generation in obese healthy women. We examined 32 healthy obese women (body mass index ≥ 28), with normal insulin sensitivity (NIS, n = 14) or impaired insulin sensitivity (n = 18), and 10 nonobese women (body mass index &lt; 25). Impaired insulin sensitivity patients had significantly higher levels of C-reactive protein (CRP), TGF-β1, plasminogen activator inhibitor-1 (PAI-1), activated factor VII (VIIa), and prothrombin fragment 1 + 2 (F1 + 2) compared with either control subjects or NIS patients. On the other hand, NIS patients had higher CRP, TGF-β1, PAI-1, and factor VIIa, but not F1 + 2, levels than controls. Significant inverse correlations were observed between the insulin sensitivity index and TGF-β1, CRP, PAI-1, factor VIIa, and F1 + 2 levels. Moreover, significant direct correlations were noted between TGF-β1 and CRP, PAI-1, factor VIIa, and F1 + 2 concentrations. Finally, multiple regressions revealed that TGF-β1 and the insulin sensitivity index were independently related to F1 + 2. Our results are the first to document an in vivo relationship between insulin sensitivity and coagulative activation in obesity. The elevated TGF-β1 levels detected in the obese population may provide a biochemical link between insulin resistance and an increased risk for cardiovascular disease.

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