IntroductIonPolycystic ovary syndrome (PCOS) may be the most common endocrine disorder of young women, affecting ~7% of women in their reproductive years (1). Hallmarks of PCOS include ovarian hyperandrogenemia (HA) and ovulatory dysfunction (2,3). The etiology of PCOS remains unclear, but hyperinsulinemia, neuroendocrine abnormalities (e.g., exaggerated luteinizing hormone (LH) secretion), and primary abnormalities of ovarian steroidogenesis have all been proposed as causes (4-6).Manifestations of PCOS often begin soon after menarche, and HA during adolescence can be a precursor of adult PCOS (7,8). However, the cause(s) of adolescent HA is (are) unclear. Obesity is a well-recognized factor in the HA of adult PCOS (9); and some (10-12) but not all (13) studies suggest that obesity is linked to HA in peripubertal girls. Therefore, obesity during the pubertal transition may be an important factor contributing to adolescent and adult PCOS (14). Although mechanisms underlying the relationship between peripubertal obesity and HA remain uncertain, early data suggest that differences of insulin and LH contribute to free testosterone (T) differences between obese and nonobese girls (11,12).Of special interest, not all peripubertal obese girls demonstrate elevated free T (12,13), suggesting that obesity per se is not sufficient to produce HA. Herein we present data that demonstrates marked variability of free T among obese girls. Furthermore, to assess potential determinants of free T elevations in obese girls, we evaluated the relationship between free T and both fasting insulin and morning LH, while simultaneously adjusting for differences in age, pubertal development, and gender-specific BMI z-score. Our primary hypotheses were that insulin and LH would be independent predictors of free T levels in obese girls. Methods and Procedures subjectsOur collaborative group collected hormonal and anthropometric data from obese girls across the pubertal spectrum. Volunteers were recruited from Endocrinology Clinics and via local advertisements and evaluated at the University of Virginia (n = 61), the University of California at San Diego (n = 8), and Yale (n = 23). Gender-specific BMI-for-age percentile (BMI%) and BMI z-score was calculated for each participant using a SAS program incorporating normative data from the National Health and Nutrition Examination Surveys

BackgroundThe purpose of this study is to assess the impact of frequency and tone of parent–youth communication on glycemic control as measured by the Family Communication Inventory (FCI). Adolescence provides a unique set of diabetes management challenges, including suboptimal glycemic control. Continued parental involvement in diabetes management is associated with improved HbA1c outcomes; however, diabetes-related conflict within the family can have adverse effects. Although it is clear that communication plays an important role in diabetes outcomes, the specific impact of frequency and tone of such communication is largely understudied.MethodsA total of 110 youths with type 1 diabetes and their parents completed questionnaires assessing diabetes-related adherence, family conflict, and family communication (i.e., frequency and tone) during a routine clinic visit. Routine testing of HbA1c was performed.ResultsYouth- and parent-reported frequency of communication were unrelated to HbA1c. Instead, greater discrepancies between parents and children on reported frequency of communication (most commonly parents reporting frequent and youth reporting less frequent communication) corresponded with poorer glycemic control and increased family conflict. More positive tone of communication as rated by youth was associated with lower HbA1c.ConclusionsDiabetes-related communication is more complex than conveyed simply by how often children and their parents communicate. Tone of communication and discrepancies in a family’s perception of the frequency of communication were better than frequency as predictors of glycemic control. The FCI appears to capture the frequency and tone of diabetes-related communication, though larger-scale studies are warranted to inform future use of this scale.Electronic supplementary materialThe online version of this article (doi:10.1007/s13300-017-0259-2) contains supplementary material, which is available to authorized users.

To evaluate the contemporary prevalence of diabetic peripheral neuropathy (DPN) in participants with type 1 diabetes in the T1D Exchange Clinic Registry throughout the U.S. RESEARCH DESIGN AND METHODSDPN was assessed with the Michigan Neuropathy Screening Instrument Questionnaire (MNSIQ) in adults with ‡5 years of type 1 diabetes duration. A score of ‡4 defined DPN. Associations of demographic, clinical, and laboratory factors with DPN were assessed. RESULTSAmong 5,936 T1D Exchange participants (mean 6 SD age 39 6 18 years, median type 1 diabetes duration 18 years [interquartile range 11, 31], 55% female, 88% non-Hispanic white, mean glycated hemoglobin [HbA 1c ] 8.1 6 1.6% [65.3 6 17.5 mmol/mol]), DPN prevalence was 11%. Compared with those without DPN, DPN participants were older, had higher HbA 1c , had longer duration of diabetes, were more likely to be female, and were less likely to have a college education and private insurance (all P < 0.001). DPN participants also were more likely to have cardiovascular disease (CVD) (P < 0.001), worse CVD risk factors of smoking (P 5 0.008), hypertriglyceridemia (P 5 0.002), higher BMI (P 5 0.009), retinopathy (P 5 0.004), reduced estimated glomerular filtration rate (P 5 0.02), and Charcot neuroarthropathy (P 5 0.002). There were no differences in insulin pump or continuous glucose monitor use, although DPN participants were more likely to have had severe hypoglycemia (P 5 0.04) and/or diabetic ketoacidosis (P < 0.001) in the past 3 months. CONCLUSIONSThe prevalence of DPN in this national cohort with type 1 diabetes is lower than in prior published reports but is reflective of current clinical care practices. These data also highlight that nonglycemic risk factors, such as CVD risk factors, severe hypoglycemia, diabetic ketoacidosis, and lower socioeconomic status, may also play a role in DPN development.Diabetic neuropathy is a prevalent complication in patients with diabetes and a major cause of morbidity and mortality (1). Among the various forms of diabetic neuropathy, distal symmetric polyneuropathy (DPN) and diabetic autonomic neuropathies are by far the most studied (1).

Day-to-night changes in LH pulse secretion are blunted in postmenarcheal obese adolescent girls. This phenomenon may in part reflect hyperandrogenemia.