This article explores the experience of Alanna Sarabia, a former San Antonio Spurs Silver Dancer, and connects it to broader discussions around weight concerns, health, and potential systemic factors influencing these aspects. It also investigates the potential impact of infectious diseases, such as arboviruses and hepatitis C virus (HCV), on metabolic changes, particularly in the context of diabetes.
Alanna Sarabia's Time as a Silver Dancer
According to a Yahoo article, Alanna Sarabia, a former San Antonio Spurs Silver Dancer (who also worked with KABB Fox 29 San Antonio and News 4 San Antonio), revealed that management expressed concerns about her weight even after she made the team. Sarabia, who danced for the Spurs from 2011 to 2012, recounted, "The night I made the team, management pulled me aside to say they were concerned about my weight." She further elaborated on the uniform situation, stating, "We were given a bin of uniforms from the year before, and I might be a solid size 6, but the girl before you might be a 2 or a 4, and that’s your uniform now - so, good luck."
After 26 seasons, the Silver Dancers were disbanded and replaced by a family-oriented co-ed "Hype Team." Reports indicated the decision was due to a lack of fan interest, a move that surprised former members of the dance team. Alanna Sarabia expressed her shock and gratitude for the support she received, stating, "I appreciate all the texts I’ve received about silver dancers and the phone calls! I truly feel all the love and I thank those who have reached out! I am trying to still process it right now. I’m just in total shock!"
The Broader Context of Weight and Health
Alanna Sarabia's experience highlights the pressures and expectations surrounding weight, particularly in industries that prioritize a specific aesthetic. While maintaining a healthy weight is important for overall well-being, the emphasis on size and appearance can sometimes overshadow the importance of individual health and fitness.
It is important to consult with medical and health professionals before adopting any suggestions or drawing inferences related to health and weight management. This publication does not render medical, health, or any other kind of personal professional services.
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The Potential Role of Infectious Diseases in Metabolic Changes
Chronic diseases, including diabetes, have surpassed infectious diseases as the dominant health concern globally. It is estimated that, by 2020, 75% of deaths in Australia will be due to chronic diseases, such as diabetes. Type 2 diabetes (T2D) also represents a significant disease burden in the Australian indigenous population, where prevalence is three times greater than that of non-indigenous Australians. Prevalence of T2D has been found to be higher in rural and remote indigenous Australian populations compared with urban indigenous Australian populations. Several studies have also found that body mass index and waist circumference are not appropriate for the prediction of T2D risk in indigenous Australians. While dietary and lifestyle factors are associated with increased risk of developing T2D, the impact of infectious diseases such as arboviruses has not been assessed.
Flaviviruses and Hepatitis C Virus (HCV)
The family Flaviviridae comprises several genera of viruses with non-segmented single-stranded positive sense RNA genomes, and includes the flaviviruses and hepaciviruses. Hepatitis C virus (HCV) has been shown to be associated with insulin resistance and subsequent development of T2D.
Flaviviruses and HCV possess conserved proteins and subgenomic RNA structures that may play similar roles in the development of insulin resistance. Regional and remote areas of Australia are endemic for a variety of mosquito-borne flaviviruses. Studies that have investigated seroprevalence of flaviviruses in remote aboriginal communities have found high proportions of seroconversion.
HCV and Insulin Resistance
Insulin resistance is a pathological feature of hepatitis C virus (HCV) infection that often leads to the development of T2D. Meta-analysis of 17 studies (N = 286,084) comparing HCV-infected individuals with uninfected individuals found an increased risk (odds ratio [OR] 1.68) of T2D in HCV-infected cases. An increased risk (OR 1.92) of T2D was also found in HCV-infected individuals compared with hepatitis B virus (HBV)-infected individuals (N = 51,156), with the association becoming greater over time. HBV is similar to HCV in targeting the liver and being capable of inducing chronic disease. However, HBV is a DNA virus from the family Hepadnavirus. A study by Mehta and others found HCV infection accelerated the onset of T2D, with development of T2D a decade earlier compared with uninfected individuals.
Available studies indicate that the HCV core protein is involved in inducing insulin resistance through alteration of insulin receptor substrate-1 pathway signalling. Studies have also demonstrated that a significant proportion of insulin resistance in HCV patients originates from extrahepatic sites. As HCV has tropism for the liver, these observations suggest that HCV infection is involved in the production of mediators capable of inducing endocrine effects at extrahepatic sites.
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Flaviviruses and Their Potential Role in Insulin Resistance
The majority of flaviviruses are mosquito-borne arboviruses. Important members include the dengue viruses, Japanese encephalitis virus, West Nile virus (WNV), and yellow fever virus. Dengue virus is among the most important flaviviruses, in terms of annual infections and morbidity. There is a substantial overlap between endemic regions and regions with increasing prevalence of T2D. Annual infections with dengue virus and other flaviviruses are increasing in the same regions, raising the question of their potential role in inducing insulin resistance and exacerbation of T2D.
Flaviviruses such as Murray Valley encephalitis virus (MVEV), Kunjin virus, Alfuy virus, Kokobera virus, Stratford virus, and Edge Hill virus are endemic to Australia and have been isolated from mosquitoes throughout Australia and the Torres Strait. Although these viruses are capable of causing human disease, the majority of infections are asymptomatic or cause only a nonspecific febrile illness. Like HCV, flaviviruses also possess a core protein and 5′ and 3′ UTRs. The 3′ UTR of flaviviruses has been shown to produce subgenomic flavivirus RNA (sfRNA). Studies have found that sfRNA is required for flavivirus pathogenicity. This sfRNA has also been shown to modulate host responses to infection via subversion of the interferon response, inhibition of cellular exoribonuclease, and suppression of the antiviral RNA interference response. However, the specific binding partners for sfRNA have not been elucidated.
Multiple amino acid sequence alignments of the core protein of members of the Flaviviridae combined with structural analysis demonstrate conservation within the N-terminal region. The N-terminal region of core protein is the region that has been found to interact with cellular proteins in addition to the UTRs in HCV. The degree of conservation in the N-terminal region of the core protein between HCV and the flaviviruses raises the possibility for a similar interaction in flavivirus infection.
MicroRNAs (miRNA) and Flaviviruses
MicroRNAs (miRNA) are generally involved in epigenetic control of expression in eukaryotes and have been found to be involved in insulin signaling, glucose metabolism, and lipid metabolism. The production of miRNA from flaviviral RNA has been predicted by computational methods. However, miRNA production has only been observed to date in vitro in mosquito cells lines infected with WNV. This particular miRNA was derived from the highly conserved distal domain of the subgenomic RNA and was determined to up-regulate expression of a host protein linked to lipid trafficking GATA-binding protein 4 GATA-4). In human and murine cell lines, GATA-4 has been demonstrated to be associated with the transcriptional regulation of the miRNA, miR-144. Interestingly, miR-144 has been linked to the development of insulin resistance and T2D.
Detection and Persistence of Flaviviral UTRs and sfRNA
Molecular assays targeting the 3′ UTR of dengue virus have demonstrated the ability to detect this target up to 10 days post-onset of fever, with this period the limit of the clinical samples assayed. The upper limit for the detection of flaviviral UTRs post-infection has not been elucidated. The sfRNA derived from flaviviral 3′ UTRs may be capable of persisting for greater periods due to their resistance to exonuclease degradation.
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Future Research Directions
The potential role of flaviviral core protein and UTRs in the development of autoimmune disease and diabetes has not yet been investigated. An important aspect in investigating the potential role of flaviviral infection in T2D pathogenesis is the determination of the extent of viral UTR and sfRNA persistence post-infection. This could be determined through a combination of screening convalescent sera from clinical samples, sera from individuals with prior diagnosed flaviviral infection, and detection in animal models post-infection. Methods developed for the detection of miRNA could be trialed for the detection of sfRNA. A variety of computational methods have been developed that could be used to predict host-binding targets for sfRNA. However, this may be limited to binding targets that have been well-researched to date.
A more conclusive method for testing the hypothesis would involve the use of animal models. A polygenic murine model of T2D has recently been developed, with mice developing the etiology and clinical criteria of human T2D based on the development of insulin resistance, concomitant dyslipidemia, and overt hyperglycemia when fed a high fat/high glycemic index diet for 20 weeks. The investigation of the effect of flaviviral infection in these mice prior to the development of clinical prediabetes and T2D, compared with that of uninfected mice, and infected and uninfected mice of the same genetic background on standard murine diet, would determine whether infection is capable of contributing to T2D development.
Diabetes in Indigenous Australians
The prevalence of T2D within the indigenous Australian community is three times higher than that of non-indigenous Australians. A systematic review of type 2 diabetes (T2D) studies surveying both rural and urban indigenous Australian populations found higher prevalence of T2D in the former compared with the latter. This result differs from prevalence surveys conducted with indigenous peoples in North America and the Pacific. The onset of T2D in non-indigenous Australians generally occurs in the mid-forties, with prevalence peaking in the age of 75 years and older cohort. For indigenous Australians, prevalence is highest in the 35- to 55-year old group. Although dietary and lifestyle factors are associated with increased risk of developing T2D, the impact of infectious diseases such as arboviruses has not been assessed. This is particularly important in light of the increased prevalence of T2D for indigenous Australians living in regional and remote areas, compared with indigenous Australians living in urban areas.