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Copyright of Medical Gazette / Medicinski Glasnik is the property of Specijalna bolnica za bolesti stitaste zlezde i bolesti metabolizma Zlatibor and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Medical Gazette / Medicinski Glasnik is the property of Specijalna bolnica za bolesti stitaste zlezde i bolesti metabolizma Zlatibor and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Medical Gazette / Medicinski Glasnik is the property of Specijalna bolnica za bolesti stitaste zlezde i bolesti metabolizma Zlatibor and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Medical Gazette / Medicinski Glasnik is the property of Specijalna bolnica za bolesti stitaste zlezde i bolesti metabolizma Zlatibor and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta ( ß ) cell dysfunction is also found in PCOS. In the study, we determined the influence of age, body mass index (BMI), and waist-to-hip ratio (WHR) on insulin response to oral glucose load (OGTT) and on insulin sensitivity (Si) and ß -cell function in young women with PCOS. One hundred fourteen patients with PCOS and 41 controls with normal basal plasma glucose were studied. A 75-g OGTT was performed to determine glucose tolerance and insulin response. Insulin sensitivity and ß -cell function were studied using a modified frequently sampled IV glucose tolerance test (FISGTT) to determine the acute insulin response (AIR G ), as well as S i by minimal model analysis. S i was decreased in PCOS women (2.49 0.18 vs. 3.41 ± 0.36, p < 0.05), but no difference in AIR G existed between the PCOS and control group (75.1 ± 4.6 vs. 63.4 ± 4.6, p < 0.05). BMI and WHR correlated negatively with S i ( r  = -0.43; r  = -0.289, p < 0.001, respectively), but not with AIR G ( r  = 0.116; r  = -0.02, p > 0.05, respectively). Increasing age correlated negatively with AIR G ( r  = -0.285, p < 0.001). There was a significant interaction between disease (PCOS), BMI, and WHR on S i as well as between age and PCOS on AIR G . Thus, patients below the age of 25 with PCOS showed enhanced AIR G (89.5 ± 7.1 vs. 65.1 ± 6.7, p < 0.05) and decreased S i (2.43 ± 0.25 vs. 4.52 ± 0.62, p < 0.05) compared to age-matched controls. In conclusion, these data suggest that not all patients with PCOS have basal and stimulated hyperinsulinemia, insulin resistance, and impaired glucose tolerance. Based on these data in young PCOS subjects, the development of insulin resistance and T2DM may be prevented with appropriate treatment strategies., Competing Interests: The authors declare that there are no conflicts of interest regarding the publication of this paper., (Copyright © 2022 Mirjana Šumarac-Dumanović et al.)

In the 20th century, the prevalence of obesity has been increasing worldwide at an alarming rate and it is followed by an increase in the diseases for which obesity is major risk factor, like metabolic syndrome, diabetes type 2 and hypertension. These facts has been resulting in explosion of investigation devoted to explanation of pathogenetic mechanisms of this serious social and medical problems with the main idea to find adequate way of prevention as well as of treatment. Together with the observed epidemy of obesity and Type 2 diabetes, it was found parallel tendency for sleep curtailment, that was confirmed in numerous epidemiological studies, that coincide with its beginning and progress with this two epidemies. This facts lead to investigations with the idea to try to explaine possible mechanisms of the association between sleep curtailment, obesity, type 2 diabetes, metabolic syndrome and polycistic ovary syndrome. Having in mind that insulin resistance is one of the fundamental pathogenetic mechanism in these disorders, numerous studies were done with the aim to explain association between sleep curtailment and insulin resistance in obesity, Type 2 diabetes, metabolic syndrome and polycistic ovary syndrome. It was demonstrated that sleep curtailment may affect energy homeostasis of human organism with the effects on body weight increase through three different ways: appetite increase, prolongation of time for food intake and through decrease of energy expenditure. There are several postulated mechanism for the effect of sleep curtailment on development of insulin resistance as well as for predisposition for Type 2 diabetes. Among possible mechanism are included: increase of sympathetic neuronal acitvity, decreased cerebral utilisation of glucose, increase in evening cortisol values, growth hormone increase and disorder of neuroendocrine control of appetite which increases the risk for getting the body weight. Metabolic systems are of particular interest in the discussion of possible mechanisms to account for elevated inflammatory mediators during sleep deprivation, particularly because of the contributory role of insulin resistance in the development of impaired vascular function and increased inflammation.