A Unique Rodent Model of Cardiometabolic Risk Associated with the Metabolic Syndrome and Polycystic Ovary Syndrome

Endocrinology ◽  
2009 ◽  
Vol 150 (9) ◽  
pp. 4425-4436 ◽  
Author(s):  
Danni Shi ◽  
Michael K. Dyck ◽  
Richard R. E. Uwiera ◽  
Jim C. Russell ◽  
Spencer D. Proctor ◽  
...  
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Cardiometabolic Risk ◽  
Polycystic Ovary ◽  
Serum Testosterone ◽  
Cardiometabolic Risk Factors ◽  
Ovary Syndrome ◽  
The Metabolic Syndrome ◽  
Ovarian Morphology

Abstract Polycystic ovary syndrome (PCOS) is characterized by hyperandrogenism, oligo-/anovulation, and polycystic ovarian morphology and is a complex endocrine disorder that also presents with features of the metabolic syndrome, including obesity, insulin resistance, and dyslipidemia. These latter symptoms form cardiometabolic risk factors predisposing individuals to the development of type 2 diabetes and cardiovascular disease (CVD). To date, animal models to study PCOS in the context of the metabolic syndrome and CVD risk have been lacking. The aim of this study was to investigate the JCR:LA-cp rodent as an animal model of PCOS associated with the metabolic syndrome. Metabolic indices were measured at 6 and 12 wk, and reproductive parameters including ovarian morphology and estrous cyclicity were assessed at 12 wk or adulthood. At 6 wk of age, the cp/cp genotype of the JCR:LA-cp strain developed visceral obesity, insulin resistance, and dyslipidemia (hypertriglyceridemia and hypercholesterolemia) compared with control animals. Serum testosterone concentrations were not significantly different between groups at 6 wk of age. However, at 12 wk, the cp/cp genotype had higher serum testosterone concentrations, compared with control animals, and presented with oligoovulation, a decreased number of corpora lutea, and an increased number of total follicles, in particular atretic and cystic follicles. The cardiometabolic risk factors in the cp/cp animals were exacerbated at 12 wk including obesity, insulin resistance, and dyslipidemia. The results of this study demonstrate that the JCR:LA-cp rodent may be a useful PCOS-like model to study early mechanisms involved in the etiology of cardiometabolic risk factors in the context of both PCOS and the metabolic syndrome.

Cardiometabolic risk factors in adolescents with polycystic ovary syndrome

2020 ◽  
Vol 26 ◽  
Author(s):  
Anastasia Vatopoulou ◽  
Maria-Eleni Dionelli ◽  
Alexis Papanikolaou ◽  
Sonia Grover
Keyword(s):  
Diabetes Mellitus ◽  
Risk Factors ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Polycystic Ovary Syndrome ◽  
Cardiometabolic Risk ◽  
Polycystic Ovary ◽  
Cardiometabolic Risk Factors ◽  
Ovary Syndrome

: It is well-established that adults with polycystic ovary syndrome (PCOS) have increased prevalence of several cardiometabolic risk factors, including obesity, insulin resistance, type 2 diabetes mellitus and dyslipidemia. Accumulating data suggest that these risk factors are already present in adolescence in patients with PCOS. This has major implications for the management of this population, since the timely identification of these risk factors is essential for preventing cardiovascular disease in adulthood. The present review summarizes the existing evidence regarding the prevalence of both traditional and non-traditional cardiometabolic risk factors in adolescents with PCOS.

Metabolic Syndrome During Menopause

2019 ◽  
Vol 17 (6) ◽  
pp. 595-603 ◽  
Author(s):  
Sezcan Mumusoglu ◽  
Bulent Okan Yildiz
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Central Obesity ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Natural Menopause ◽  
The Metabolic Syndrome ◽  
Increased Risk ◽  
Aging Women

The metabolic syndrome (MetS) comprises individual components including central obesity, insulin resistance, dyslipidaemia and hypertension and it is associated with an increased risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). The menopause per se increases the incidence of MetS in aging women. The effect(s) of menopause on individual components of MetS include: i) increasing central obesity with changes in the fat tissue distribution, ii) potential increase in insulin resistance, iii) changes in serum lipid concentrations, which seem to be associated with increasing weight rather than menopause itself, and, iv) an association between menopause and hypertension, although available data are inconclusive. With regard to the consequences of MetS during menopause, there is no consistent data supporting a causal relationship between menopause and CVD. However, concomitant MetS during menopause appears to increase the risk of CVD. Furthermore, despite the data supporting the association between early menopause and increased risk of T2DM, the association between natural menopause itself and risk of T2DM is not evident. However, the presence and the severity of MetS appears to be associated with an increased risk of T2DM. Although the mechanism is not clear, surgical menopause is strongly linked with a higher incidence of MetS. Interestingly, women with polycystic ovary syndrome (PCOS) have an increased risk of MetS during their reproductive years; however, with menopausal transition, the risk of MetS becomes similar to that of non-PCOS women.

scholarly journals Association of intraocular pressure with the metabolic syndrome and novel cardiometabolic risk factors

Eye ◽  
2009 ◽  
Vol 24 (6) ◽  
pp. 1037-1043 ◽  
Author(s):  
Y C Chang ◽  
J-W Lin ◽  
L C Wang ◽  
H M Chen ◽  
J J Hwang ◽  
...  
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Intraocular Pressure ◽  
Cardiometabolic Risk ◽  
Cardiometabolic Risk Factors ◽  
The Metabolic Syndrome

Polycystic ovary syndrome: reproductive aspects

2011 ◽  
pp. 1229-1234
Author(s):  
Sophie Catteau-Jonard ◽  
Cécile Gallo ◽  
Didier Didier
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Reproductive Age ◽  
Therapeutic Approaches ◽  
Women Of Reproductive Age ◽  
Ovary Syndrome ◽  
Common Cause ◽  
The Metabolic Syndrome

The polycystic ovary syndrome (PCOS) is the most common cause of anovulation and hyperandrogenism in women, affecting between 5 and 10% of women of reproductive age worldwide (1). Although this difficult topic in endocrine gynaecology is under extensive research, controversies still remain about the pathophysiology, diagnosis, and therapy of PCOS. The PCOS phenotype can be structured in three components: manifestations of anovulation, hyperandrogenism, and the metabolic syndrome (of which hyperinsulinaemia secondary to insulin resistance is the central abnormality). The latter two are addressed in other chapters. Our knowledge about the mechanism of disturbed folliculogenesis in PCOS that is responsible for its reproductive aspects has much increased these last years, thus opening new avenues for the diagnostic and therapeutic approaches.

scholarly journals The Polycystic Ovary Syndrome and the Metabolic Syndrome: A Possible Chronobiotic-Cytoprotective Adjuvant Therapy

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Eduardo Spinedi ◽  
Daniel P. Cardinali
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Polycystic Ovary Syndrome ◽  
White Adipose Tissue ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
The Metabolic Syndrome ◽  
Obstructive Sleep ◽  
The Impact

Polycystic ovary syndrome is a highly frequent reproductive-endocrine disorder affecting up to 8–10% of women worldwide at reproductive age. Although its etiology is not fully understood, evidence suggests that insulin resistance, with or without compensatory hyperinsulinemia, and hyperandrogenism are very common features of the polycystic ovary syndrome phenotype. Dysfunctional white adipose tissue has been identified as a major contributing factor for insulin resistance in polycystic ovary syndrome. Environmental (e.g., chronodisruption) and genetic/epigenetic factors may also play relevant roles in syndrome development. Overweight and/or obesity are very common in women with polycystic ovary syndrome, thus suggesting that some polycystic ovary syndrome and metabolic syndrome female phenotypes share common characteristics. Sleep disturbances have been reported to double in women with PCOS and obstructive sleep apnea is a common feature in polycystic ovary syndrome patients. Maturation of the luteinizing hormone-releasing hormone secretion pattern in girls in puberty is closely related to changes in the sleep-wake cycle and could have relevance in the pathogenesis of polycystic ovary syndrome. This review article focuses on two main issues in the polycystic ovary syndrome-metabolic syndrome phenotype development: (a) the impact of androgen excess on white adipose tissue function and (b) the possible efficacy of adjuvant melatonin therapy to improve the chronobiologic profile in polycystic ovary syndrome-metabolic syndrome individuals. Genetic variants in melatonin receptor have been linked to increased risk of developing polycystic ovary syndrome, to impairments in insulin secretion, and to increased fasting glucose levels. Melatonin therapy may protect against several metabolic syndrome comorbidities in polycystic ovary syndrome and could be applied from the initial phases of patients’ treatment.

scholarly journals Cardiometabolic risk in polycystic ovary syndrome: a comparison of different approaches to defining the metabolic syndrome

2008 ◽  
Vol 23 (10) ◽  
pp. 2352-2358 ◽  
Author(s):  
A. J. Cussons ◽  
G. F. Watts ◽  
V. Burke ◽  
J. E. Shaw ◽  
P. Z. Zimmet ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Polycystic Ovary Syndrome ◽  
Cardiometabolic Risk ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
The Metabolic Syndrome

scholarly journals Irregularity of energy intake at meals: prospective associations with the metabolic syndrome in adults of the 1946 British birth cohort

2015 ◽  
Vol 115 (2) ◽  
pp. 315-323 ◽  
Author(s):  
Gerda K. Pot ◽  
Rebecca Hardy ◽  
Alison M. Stephen
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Waist Circumference ◽  
Energy Intake ◽  
Cardiometabolic Risk ◽  
Cardiometabolic Risk Factors ◽  
Logistic Regression Models ◽  
The Metabolic Syndrome ◽  
Increased Risk ◽  
Health And Development

AbstractIrregularity in eating patterns could be a potential cardiometabolic risk factor. We aimed to study the associations of irregular intake of energy at meals in relation to cardiometabolic risk factors 10 and 17 years later. Variability of energy intake data – derived from 5-d estimated diet diaries of cohort members of the National Survey for Health and Development collected at ages 36 (n1416), 43 (n1505) and 53 years (n1381) – was used as a measure for irregularity. Associations between meal irregularity scores with cardiometabolic risk factors measured 10 and 17 years later were investigated using linear mixed models and logistic regression models. The results showed that irregularity scores changed significantly over the years (P<0·05). At age 36 years, subjects with a more irregular intake of energy at lunch (OR 1·42; 95 % CI 1·05, 1·91) and between meals (OR 1·35; 95 % CI 1·01, 1·82) had an increased risk for the metabolic syndrome 17 years later; at lunch was also associated with an increased waist circumference (OR 1·58; 95 % 1·27, 1·96) and TAG levels (OR 1·33; 95 % CI 1·02, 1·72). At age 43 years, subjects with a more irregular intake at breakfast had an increased risk of the metabolic syndrome 10 years later (OR 1·53; 95 % CI 1·15, 2·04), as well as an increased BMI (OR 1·66; 95 % CI 1·31, 2·10), waist circumference (OR 1·53; 95 % CI 1·23, 1·90) and diastolic blood pressure (OR 1·42; 95 % CI 1·13, 1·78). In conclusion, subjects with a more irregular intake of energy, mostly at breakfast and lunch, appeared to have an increased cardiometabolic risk 10 and 17 years later.

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