Browsing by Subject "Diabetes Mellitus, Type 2"
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Item Assessing Self-Care Perception in Patients Living with Type 2 Diabetes and Their Physicians(2021-05-01T05:00:00.000Z) Balakrishnan, Naveen Kishore; Day, Philip; Kale, Neelima; Schneider, DavidBACKGROUND: Type 2 diabetes mellitus (T2D) is chronic illness affecting millions in the United States. Patients living with T2D require highly individualized care and significant patient effort. This effort is comprised of the patient's self-care with regards to medication, diet, lifestyle, and mental health. Self-efficacy is a patient's ability to feel agency over their illness and therefore feel able to maintain self-care. Previous literature suggests that improving a patient's self-efficacy through various behavioral health interventions may improve a patient's ability to manage their T2D. Additionally, interventions on self-efficacy are thought to work regardless of health literacy level and might be a generalizable intervention. However, while validated surveys assessing patient diabetes distress, quality-of-life, social determinants of health, adverse childhood events, and more exist, no literature was found attempting to understand a patient's perspective on their self-care, and by extension, their self-efficacy. Under the premise that consistent beliefs between patient and physician regarding self-care are necessary to make meaningful plans promoting self-care and self-efficacy, the authors developed the term self-care perception consistency to assess relationship between patient and physician perceptions of a patient's self-care. OBJECTIVE: The objective is to assess the consistency between patient and physician perceptions of patient self-care through a biopsychosocial and structural/social determinants of health lens. METHODS: This study uses a cross-sectional, quantitative data set obtained by the Research Residency Network of Texas (RRNeT) through a 71-item survey study. This survey was completed across 12 Family Medicine residencies in Texas and included individuals between 18-75 who were living with T2D. Responses ranged from short free response to Likert-scale based questions and covered topics such as demographics, social determinants of health, patient self-care, diabetes distress, quality-of-life, adverse childhood events, and more. The physicians of each patient were asked to complete a shorter 10-item survey with broader analogous questions to the patient survey. This data was collected through RedCap and analyzed through RStudio. RESULTS: The term self-care perception consistency was coined to describe the relationship between the patient's and physician's perception of the patient's self-care. Self-care perception consistency was found to be lacking 31.2% of the time. Only HgA1c (p<0.01) was inversely correlated with self-care perception consistency in both the univariate and multivariate analyses of demographic factors and social determinants of health. Additional analysis was completed to assess the relationship of HgA1c control, patient diabetes distress, patient quality-of-life, and the physician survey with self-care perception consistency. Self-care perception consistent and inconsistent groups were found to have significantly different HgA1c control distributions (p < 0.01) in the subset of patients that rated their self-care positively, but no significant difference was found in the group that rated their self-care negatively. Patient self-care ratings were best correlated with their diabetes distress (p<0.01) and HgA1c (p<0.01) while physician ratings of patient self-care were best correlated with their perception of HgA1c, perception of patient diabetes distress, perception of patient quality-of-life, and perception of patient social connectedness (p<0.01 for all). Notably, trending diabetes distress, quality-of-life, the physician survey, and social determinants of health across patient self-care ratings in self-care perception consistent versus inconsistent groups revealed that only the physician survey showed opposite trends across the consistent and inconsistent groups. CONCLUSION: Self-care perception consistency was found to be lacking 31.2% of the time. Notably, HgA1c is correlated with patient and physician perceptions of patient self-care (p<0.01 for both); however, in instances of patient-physician self-care perception inconsistency, HgA1c is not correlated with patient self-care perception. Instead, diabetes distress remains predictive of patient self-care rating in all instances (p<0.01). Patient-physician self-care perception inconsistency is also associated with inconsistency in patient and physician perceptions of the patient's diabetes distress. As diabetes distress remains consistently correlated with patient self-care rating, using the validated diabetes distress survey-17 with an additional question regarding self-care may help physicians better understand patients and therefore target appropriate education and psychosocial interventions.Item Bariatric surgery for the treatment of type 2 diabetes(2013-06-14) Lingvay, IldikoItem The bHLH/PAS Transcription Factor SIM1 Is a Novel Obesity Gene(2005-05-03) Holder, Jimmy Lloyd, Jr.; Zinn, Andrew R.Obesity is epidemic in the United States and other developed countries. Obesity is a major risk factor for type II diabetes, hypertension, hyperlipidemia and osteoarthritis. I report a unique girl with early-onset obesity (47.5 kg, +9.3 s.d. above mean at age 67 months) and a de novo balanced translocation between chromosomes 1 and 6. She has normal energy expenditure and a voracious appetite. I show that her translocation disrupts a transcription factor gene, SIM1, on chromosome 6q16.2. I also present data that Sim1 haploinsufficiency causes obesity in mice. Animals heterozygous for a Sim1 null allele fed a standard chow diet (4% fat) developed obesity around the time of sexual maturity, were 33-45% heavier than wild-type littermates by 5 months of age, and had increased adiposity by DEXA scans. In contrast, the human subject developed obesity by two years of age, well before puberty. To investigate whether differences in dietary fat consumption might explain this discrepancy in human and mouse phenotypes, I fed mutant mice and wild type littermates a "Westernized" diet (35% fat). Heterozygous Sim1 mice fed this diet became obese prior to 6 weeks of age. The obesity was also more severe, especially in females, who by 8 weeks of age weighed 72% more than controls compared with 13% on a low fat diet. Heterozygous Sim1 mice maintained on a 4% fat diet ate more than controls over a 5 day period (delta kcals 12-14%), and became even more hyperphagic when acutely challenged with increased dietary fat (delta kcals 46-68% over 5 days). This altered behavior was evident within the first day of exposure to the high fat diet: during this time, heterozygous Sim1 mice failed to significantly change the mass of food consumed, whereas wild-type littermates decreased their food consumption by >15%. These data suggest that Sim1 is critical for the acute and chronic homeostatic response to elevated dietary fat. This data demonstrates that normal Sim1 gene dosage is critical for proper regulation of feeding behavior and body weight regulation.Item Cardiogenic diabetes and related puzzles(2006-01-12) Malloy, Craig R.Item Interactive Effects of Obstructive Sleep Apnea and Type 2 Diabetes Mellitus on Corneal Nerves: Preliminary Findings(2017-01-17) Stuard, Whitney; Gallerson, Bryan; Robertson, Danielle M.INTRODUCTION: In vivo corneal confocal microscopy (IVCM) is increasingly being used to evaluate the corneal subbasal nerve plexus (SBNP) in patients with Type 2 Diabetes Mellitus (T2DM). Current data suggests that loss of the SBNP is a surrogate marker for peripheral diabetic neuropathy (DPN). Obstructive Sleep Apnea (OSA) is an under diagnosed condition that is highly prevalent in patients with T2DM. The purpose of this study is to examine the impact of OSA on SBNP changes in patients with T2DM. METHODS: A total of 184 patients will be recruited across four groups: A) T2DM and OSA, 2) OSA, 3) T2DM, and 4) healthy controls. A physician diagnosis of T2DM and/or OSA is required for inclusion in each study group. Groups are matched for sex, age, and obesity status. Each patient undergoes testing for the following: serology for Hemoglobin A1c and high sensitivity C-reactive protein, an eye exam with dry eye testing and dilated fundus examination, anthropometric measurements, tear collection, IVCM, measurement of corneal sensitivity, and optical coherence tomography to assess the retinal nerve fiber layer (rNFL) and macula. Patients are also asked to complete three questionnaires including the Stop-Bang questionnaire (to assess risk of OSA), the ocular surface disease index questionnaire (to assess dry eye disease), and a CPAP compliance survey. IVCM images are analyzed for determination of nerve fiber length and density, tortuosity (short term and long term), and basal corneal epithelial cell and dendritic cell density. Human tears are analyzed for tear levels of IGFBP3 using ELISA and extracellular tear DNA is quantified using a Qubit Fluorometer. Anthropometric measurements are used to calculate body mass index and waist to height ratio. RESULTS: Preliminary data confirms that Hemoglobin A1c is highest in the two groups with T2DM patients; STOP BANG scores and male neck circumference are highest in the two groups with OSA. Nerve fiber length is shortest in patients with T2DM. Tortuosity and morphological differences have been found amongst the four groups. A slight decrease has been found in the rNFL for patients with OSA and T2DM. DISCUSSION: A recent study in the UK analyzed the risk and severity of DPN in patients with OSA. Among 266 patients with T2DM, those with OSA had a higher prevalence of DPN and the severity of neuropathy was related to the severity of OSA and not the duration of T2DM. The results of the present study will be the first to show a definitive relationship in changes in the SBNP and rNFL between patients with OSA and T2DM.Item Item [News](1988-01-21) Bosler, Tommy JoyItem [News](1988-10-14) Bosler, Tommy JoyItem [News](1990-02-28) Bosler, Tommy JoyItem The non-calciotropic actions of vitamin D: modulation of cardiovascular, immune and proliferative disorders(2007-11-30) Maalouf, NaimItem Regulating drugs that regulate glucose: cardiovascular assessment of type 2 diabetes medications(2014-10-17) McGuire, Darren K.Item Role of Ceramide Accumulation in the Ventromedial Hypothalamus in Driving Systemic Metabolic Impairments During Obesity(2019-03-01) Johnson, Joshua A.; Williams, Kevin W.; Elmquist, Joel; Zigman, Jeffrey M.; Holland, William L.Obesity remains a tremendous national and global health epidemic and causes increased risk for any number of serious diseases. In the field of obesity, the idea of lipotoxicity (accumulation of toxic lipids in cells unable to handle them) has become an accepted concept, with increases in tissue lipids being recognized to cause tissue dysfunction during obesity. One of these lipotoxic lipids is ceramide, a sphingolipid. Ceramides have been demonstrated to blunt insulin sensitivity and contribute to numerous obesity-related impairments of tissue function, as seen in vascular endothelium, pancreatic islets, heart failure, and muscle, liver, and adipose insulin signaling. Recently, it has been shown that during obesity ceramides accumulate in the hypothalamus, the region of the brain known to regulate many aspects of metabolism. As hypothalamic lipid metabolism is rapidly being established as a key player in whole-body metabolic homeostasis, we became interested in whether this ceramide accumulation in the brain is another avenue via ceramide accumulation during obesity causes its numerous deleterious effects. To study this, we have overexpressed acid ceramidase in neurons in the ventromedial hypothalamus (VMH); this will decrease ceramide content specifically in this brain region vital to the control of glucose homeostasis and body weight. We found that ceramide accumulation in the VMH during obesity drives glucose intolerance without changing body weight or insulin sensitivity, and that this effect is due to an increase in glucagon sensitivity. Furthermore, we have included a general investigation on ceramide synthesis in response to high fat diet, as well as a blueprint for future studies of sphingolipid metabolism in the brain.Item The Role of Hypertension and Type II Diabetes in Glaucoma Severity(2021-05-01T05:00:00.000Z) Tong, Betty Le; Kooner, Karanjit; Petroll, W. Matthew; Chiu, MichaelBACKGROUND: Hypertension (HTN) and Type II Diabetes (DM) are risk factors associated with the development of primary open angle glaucoma (POAG), but the effects of these diseases on POAG severity are not well known. OBJECTIVE: To evaluate for differences in glaucoma severity for patients with (1) HTN alone, (2) DM alone, (3) both HTN and DM, and (4) neither HTN nor DM. METHODS: In this IRB approved retrospective chart review study, we selected a total of 767 patients with POAG or ocular hypertension (OHT) seen at UT Southwestern Aston eye clinic in Dallas, Texas. The inclusion criteria were patients who were > 18 years old, had open angles, and no evidence of secondary glaucoma or retinal/optic nerve pathologies. Variables collected included: visual acuity, intraocular pressure, central corneal thickness, visual fields, blood pressure, HgbA1c, demographic factors (age, race, gender), and optic coherence tomography angiography (OCTA) data such as mean macular vessel density (VD), peripapillary VD, peripapillary retinal nerve fiber layer (RNFL), and total ganglion cell complex (GCC). RESULTS/CONCLUSION: Out of a total of 1104 participants reviewed, we selected 767. Among the included patients, there were 149 (19.5%) subjects without POAG, 122 (15.9%) with OHT, 95 (12.4%) with mild POAG, 137 (17.9%) with moderate POAG, and 262 (34.2%) with severe POAG. Regarding the four comorbid disease groups of interest, there were 212 (27.6%) control patients with neither HTN nor DM, 318 (41.5%) with HTN alone, 47 (6.1%) with DM alone, and 190 (24.8%) with both HTN and DM. All comorbidity groups had more female than male, and the average age of the groups ranged from 66-72 years old. We did not find a significant difference in the distribution of glaucoma severity between those with HTN/DM and those without. OCTA analysis corroborated our findings.Item Role of the Vitamin D Receptor in Insulin Secretion and Beta Cell Function(2012-07-20) Kjalarsdottir, Lilja; Repa, Joyce J.1,25-dihydroxyvitamin D3 (VitD) is a ligand for the Vitamin D Receptor (VDR, NR1I1), which is a member of the family of Nuclear Hormone Receptors (NHR). Previously, the Repa lab identified VDR as the fourth most abundant NHR in mouse islets based on mRNA levels, also, VDR is clearly present in human islets [1]. In the past years multiple epidemiological studies have implicated Vitamin D deficiency in the development of Type 2 Diabetes, however no reports have described any mechanism(s) linking VitD status with pancreatic islet function. Therefore, my studies have focused on the role of Vitamin D and VDR in islet biology. Preincubation of isolated mouse and human islets with Vitamin D results in enhanced glucose-stimulated insulin secretion (GSIS). This response is VDR-dependent, as no VitD-mediated change in GSIS is observed in islets obtained from Vdr-null mice. However, VitD causes no changes in gene expression of any of the major islet hormones, nor does it change glucose uptake into primary beta cells. VitD does however increase glucose-stimulated calcium uptake, suggesting that VitD affects transcription of genes involved in calcium flux into the beta cell. To identify molecular mechanisms linking VDR activity to increased insulin secretion and increased glucose-stimulated calcium uptake, we performed global gene expression profiling by microarray in mouse and human islets. These studies identified multiple genes associated with islet function, calcium transport and insulin secretion. One of these genes is the R-type voltage-gated calcium channel, CaV2.3, which is highly upregulated by VitD in human and mouse islets. We identified a strong VDR binding element within intron 7 of the Cav2.3 gene that is conserved in mouse and man. With previous reports linking Cav2.3 activity with Type 2 Diabetes, our findings support a role for vitamin D signaling in the regulation of CaV2.3 and calcium uptake to enhance glucose-stimulated insulin secretion by beta cells of the endocrine pancreas. A second VDR target gene we identified in the islet is klotho, a key regulator of phosphate homeostasis. We clearly establish that klotho mRNA and protein are detected in beta cells of mouse islets, at levels sufficient to mediate signal transduction pathways via klotho’s role as a co-receptor for FGF23. By analysis of islets from Klotho-/- mice, we also show that the sialidase activity of klotho may modulate the membrane localization of GLUT-2 to affect glucose-stimulated insulin secretion. In summary, my studies suggest that vitamin D status may impact the beta cell’s capacity to sense glucose levels and respond appropriately to secrete the anabolic hormone, insulin. Future studies involving beta cell-selective deletion of VDR, klotho, and Cav2.3 are now warranted, to elucidate the contribution of islet vitamin D signaling pathways in glucose homeostasis in vivo. The results of studies for my dissertation research provide a needed mechanistic approach, which complements the current clinical and observational reports that exist, regarding potential roles for Vitamin D in the progression of Diabetes. In addition, our identification of numerous Vitamin-D regulated genes of the human and mouse islet can form the basis for future hypothesis-driven research efforts to identify novel therapeutic targets to affect insulin secretion and beta cell function.Item SGLT 2 inhibitors improve cardiorenal outcomes in DM2 -- get rid of the sugar(2017-10-06) Balis, David S.Item SIRT6 Overexpression Protects Against Diet-Induced Diabetes in Mice(2013-08-13) Anderson, Jason Graham; Scherer, Philipp; Elmquist, Joel; Coppari, Roberto; Elias, Carol; Kuro-O, MakotoNumerous studies in a variety of species indicate that caloric restriction (CR) elicits beneficial metabolic effects including reduced adiposity and improved glucose homeostasis, as well as enhanced insulin and leptin sensitivity. Conversely, chronic feeding on high caloric diets brings about opposite outcomes and can progress to type-II-diabetes and obesity. An intense effort by many researchers has begun to elucidate the homeostatic mechanisms accounting for these beneficial metabolic effects of CR in order to facilitate development of CR-mimetic drugs to combat the alarming increase of these diseases. Mounting experimental evidence suggests that Sirtuins may be principal mediators of the metabolic effects of CR (1). Sirtuins are believed to sense and respond to cellular energy deficit via their (NAD+)-dependent enzymatic activities including lysine deacetylation of a variety of cytosolic, mitochondrial and nuclear proteins (2). Initial studies involving SIRT6, one of three nuclear sirtuins, suggest that it may be an attractive drug target for obesity and type-II-diabetes therapy. Knockout studies indicate that SIRT6 is required for normal growth, adiposity, and glucose homeostasis (3). Yet, contrasting these Sirt6-null phenotypes with those from opposing SIRT6 gain-of-function animal models lead to incongruous and seemingly contradictory conclusions regarding the stress-responsive homeostatic functions of SIRT6, casting doubt as to whether SIRT6 agonist or antagonist drugs should be sought after. To address these issues, I generated genetically engineered mice (Sirt6BAC mice) designed to eutopically overexpress SIRT6 and mimic its moderate eutopic upregulation observed during CR. This was achieved via BAC- mediated genomic insertion of an isogenic 187kb DNA region from chromosome 10 of mus musculus encompassing Sirt6. These Sirt6BAC mutants fed a high caloric diet exhibit improved glucose homeostasis as indicated via intraperitoneal glucose tolerance tests and intraperitoneal pyruvate tolerance tests. Hyperinsulinemic/euglycemic clamp indicate that these mutants exhibit enhanced insulin-sensitive inhibition of endogenous glucose production as well as enhanced blood glucose disposal and uptake into gastrocnemius and soleus muscle. Importantly, these data suggest that SIRT6 agonist drugs may be worthy of translational research for the treatment of type-II diabetes in humans.Item [Southwestern News](2005-03-25) Hansard, Donna StephItem [Southwestern News](2004-06-16) Hansard, Donna StephItem [Southwestern News](2004-06-26) O'Brien, StephenItem [Southwestern News](1997-04-29) Steeves, Susan A.