ABSTRACT THE EFFECTS OF HIV DISEASE AND LIFESTYLE FACTORS ON CELLULAR AGING IN TRANSGENDER WOMEN by Scott Stephen Sohn Background: Telomeres are short tandem repeats of nucleotides at the ends of chromosomes. These specialized structures serve as caps on the end of the chromosomes, which protect DNA integrity. Telomeres get shorter each time a cell replicates, but the DNA remains intact as long as the telomere caps are a sufficient length. In time, telomeres become too short to protect DNA, which leads to cellular death. Previous research has shown that disease and negative lifestyle factors play a role in accelerated telomere attrition throughout the cellular life cycle. Objective: The purpose of this study was to determine if HIV infection and lifestyle factors in a transgender population living in Atlanta Georgia are associated with telomere length reduction. Participants/setting: This study is a secondary analysis of data provided by a Georgia State University study entitled “Telomere Length, Environmental Stressors and Health Related Outcomes among Transgender Women”. The study included 92 transgender women from Atlanta, Georgia with 49 reporting HIV infection. Two sources of data were collected, survey responses collected during face to face interviews and a saliva sample for DNA analysis. Statistical analysis: Frequency statistics were used to describe the sample population. A Mann Whitney U was used to evaluate telomere length using the T/S ratio by HIV status, by physical activity level (healthy active or low active) and by fruit and vegetable intake category (Don’t eat, 1-2 servings/day, 3-4 servings/day vs. >5 servings/day) in the total Population. Multiple regression analysis was used to examine the association between independent variables (activity level, body mass index, fruit and vegetable intake, hormone use, race, HIV status and age) and telomere length. Results: The majority of the population was Black (84%) with a median age of 33 years (range, 18 to 65 years). No significant association was observed between HIV infection and T/S ratio. The vast majority of the population reported low activity level and only 9% reported consuming >5 servings of fruits and vegetables daily. No significant association was found between fruit and vegetable intake or physical activity level and T/S ratio in this population. Conclusion: HIV infection, Fruit and vegetable intake, and physical activity were not found to impact telomere length in an urban population of transgender women. Future research is needed to further understand the mechanisms that impact telomere length throughout the cellular life cycle within the transgender population.

Bakgrund: Negativ kroppsuppfattning,intryck av dagens kroppsideal och påverkan från media är riskfaktorer som kan leda till att ungdomar utvecklar ett ohälsosamt bantningsbeteende. Där förhoppningen är att gå ned i vikt på ett eller annat sätt med hjälp av sjukdomsalstrande bantningsmetoder. Konsekvenser av ett ohälsosamt bantningsbeteende kan leda resultera i att ungdomar äventyrar sin hälsa både fysiskt och psykiskt. Eftersom ohälsosamma bantningsbeteenden ökar kraftigt hos ungdomar skapar detta ett behov för skolsköterskan och elevhälsan att utveckla och genomföra förebyggande insatser för att tidigt kunna upptäcka och effektivt hantera ett ohälsosamt bantningsbeteende hos elever. Syfte: Syftet med studien var att beskriva skolsköterskans erfarenheter av att arbeta med ohälsosamma bantningsbeteenden hos ungdomar. Metod: En kvalitativ ansats användes. Personliga semistrukturerade intervjuer gjordes med tio skolsköterskor. Intervjuerna analyserades utifrån en kvalitativ innehållsanalys. Resultat: Resultatet visas i from av fyra kategorier: identifera varningstecken, samverkan med föräldrar, samverkan i och utanför elevhälsan, samt förhålla sig professionellt. Resultatet visade främst likheter, men även skillnader i skolsköterskans erfarenheter av ett ohälsosamt bantningsbeteende hos elev. Slutsats: För att främja hälsa hos elev bör skolsköterskan tidigt identifiera varningstecken, arbeta mera familjefokuserat samt förbättra samarbetet med elevhälsan och andra vårdverksamheter. Ett förslag till förbättring är utformning av riktlinjer som kan användas som stöd för tillvägagångsätt.

The purpose of this research was to determine whether adipocytes express ACE2 and its role in obesity-associated hypertension with diet-induced obesity. To determine if ACE2 was expressed in adipose tissue and its regulation in the setting of diet-induced obesity, we fed male mice either a low fat (LF) or high fat (HF) diet acutely (1 week) or chronically ( 4 months). We demonstrated that ACE2 was regulated specifically in adipose tissue with consumption of a HF diet. However, with chronic HF feeding adipose ACE2 was dysregulated resulting in activation of the systemic RAS and increased blood pressure. To determine the role of ACE2 in obesity-associated hypertension, we used ACE2 deficient male and female mice. Wild type and ACE2 deficient mice were chronically fed either a LF or HF diet. Metabolic parameters were measured during the entire course of the study and blood pressure was measured by telemetry at the end of the study. Results from these studies demonstrate that HF diet promotes obesity-associated hypertension in male mice which is further augmented with ACE2 deficiency. Further, ACE2 deficiency resulted in marked glucose intolerance suggesting that stimulation of ACE2 may blunt the progression of obesity-associated diabetes. In contrast to the males, females are protected against obesity-associated hypertension. However, this protection in the females is lost with ovariectomy and ACE2 deficiency. These results suggest that female sex hormones protect the females against obesity-associated hypertension by regulating ACE2. To define mechanisms for HF diet-induced regulation of ACE2 in adipose tissue we examined various fatty acids for their ability to regulate ACE2 mRNA abundance in 3T3-L1 adipocytes. We revealed that omega-3 fatty acids, known regulators of PPARγ, increased ACE2 mRNA abundance in adipocytes. Therefore, we examined in vitro and in vivo regulation of ACE2 in 3T3-L1 cells and adipose tissue by PPARγ receptor ligands (TZDs). Results demonstrate regulatory effects of PPARγ to promote ACE2 gene transcription. These effects were associated with changes in glucose tolerance. Taken together, these results demonstrate that adipose ACE2 plays a protective role against obesity-associated hypertension in male and female mice and is regulated by natural and synthetic ligands of PPARγ.

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