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Regulation of Insulin Receptor Pathway and Glucose Metabolism by CD36 Signaling.
Samovski D, Dhule P, Pietka T, Jacome-Sosa M, Penrose E, Son NH, Flynn RC, Shoghi KI, Hyrc KL, Goldberg IJ, Gamazon ER, Abumrad NA
(2018) Diabetes :
Show Abstract · Added May 26, 2018
During reduced energy intake, skeletal muscle maintains homeostasis by rapidly suppressing insulin-stimulated glucose utilization. Loss of this adaptation is observed with deficiency of the fatty acid transporter CD36. A similar loss is also characteristic of the insulin resistant state where CD36 is dysfunctional. To elucidate what links CD36 to muscle glucose utilization we examined whether CD36 signaling might influence insulin action. First, we show that CD36 deletion specific to skeletal muscle reduces expression of insulin signaling and glucose metabolism genes. It decreases muscle ceramides but impairs glucose disposal during a meal. Second, in primary-derived human myotubes depletion of CD36 suppresses insulin signaling and the mechanism is shown to involve functional CD36 interaction with the insulin receptor (IR). CD36 promotes tyrosine phosphorylation of IR by the Fyn kinase, enhances IR recruitment of P85 and downstream signaling. Third, pretreatment for 15 minutes with saturated fatty acids suppresses CD36-Fyn enhancement of IR phosphorylation, while unsaturated fatty acids are neutral or stimulatory. These findings define mechanisms important for muscle glucose metabolism and optimal insulin responsiveness. Potential human relevance is suggested by GWA RNA-Seq data that associate genetically determined low muscle CD36 expression to incidence of diabetes type 2.
© 2018 by the American Diabetes Association.
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1 Members
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0 MeSH Terms
Sleep habits in adolescents with type 1 diabetes: Variability in sleep duration linked with glycemic control.
Patel NJ, Savin KL, Kahanda SN, Malow BA, Williams LA, Lochbihler G, Jaser SS
(2018) Pediatr Diabetes :
Show Abstract · Added May 18, 2018
OBJECTIVE - To describe adolescents' sleep on school and weekend nights using multiple methods and to examine the links between sleep variability, quality, and duration with diabetes indicators.
METHODS - Adolescents with type 1 diabetes (N = 65, mean age = 15.0, 52.3% female, mean HbA1c = 8.9% or 74 mmol/mol) wore an actigraph and kept daily diaries recording sleep, activities, and blood glucose monitoring (BGM) habits for at least 7 days. Average daily BGM and blood glucose (BG) levels were obtained through glucometer downloads. HbA1c was obtained as part of clinic visits. Adolescents completed a sleep quality questionnaire (Pittsburgh sleep quality index [PSQI]), and adolescents and caregivers reported on adherence to diabetes treatment.
RESULTS - Adolescents reported a mean PSQI global score of 5.37, which is above the clinical cutoff for poor sleep quality. Actigraphy data revealed that mean adolescent total sleep time was 6:54 (h:min), and participants slept more on weekend nights than on school nights (P < .001). Additionally, variability in sleep duration was significantly related to HbA1c, frequency of BGM, and average BG. Total sleep time and self-reported sleep quality were not significantly associated with adherence or glycemic control.
CONCLUSIONS - Few adolescents with type 1 diabetes met recommendations for sleep duration, and many reported poor sleep quality. We identified significant associations between variability in sleep duration with poorer glycemic control and less frequent BGM, supporting the need to consider sleep patterns as a modifiable factor that may affect adherence and glycemic control.
© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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Measures of Adherence and Challenges in Using Glucometer Data in Youth with Type 1 Diabetes: Rethinking the Value of Self-Report.
Datye KA, Patel NJ, Jaser SS
(2017) J Diabetes Res 2017: 1075428
Show Abstract · Added May 18, 2018
Purpose - The current study compares the relative strength of associations of different adherence measures with glycemic control in adolescents with type 1 diabetes, while highlighting the challenges in using more objective measures (i.e., glucometer data).
Methods - Adolescents with type 1 diabetes ( = 149) and their caregivers completed a questionnaire measure assessing adolescents' adherence (Self-Care Inventory (SCI)) to the diabetes regimen. Adolescents' glucometers were downloaded to determine average blood glucose checks per day, as an objective measure of adherence. A measure of glycemic control (hemoglobin A1c (HbA1c)) was obtained as part of adolescents' regular clinic visits.
Results - Adolescents' self-reported adherence to the treatment regimen was more strongly correlated with HbA1c than caregivers' reports of adherence. In multivariate analyses, both adolescents' self-report of adherence and average blood glucose checks per day (obtained via a glucometer) were significant predictors of HbA1c. Challenges to obtaining glucometer data were identified.
Conclusions - The findings highlight adolescents' self-report of adherence using the SCI as a brief and meaningful measure to understand and improve adolescents' glycemic control, particularly when glucometer data is difficult to obtain.
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Long-term Diet Quality and Risk of Type 2 Diabetes Among Urban Chinese Adults.
Yu D, Zheng W, Cai H, Xiang YB, Li H, Gao YT, Shu XO
(2018) Diabetes Care 41: 723-730
Show Abstract · Added March 26, 2018
OBJECTIVE - Little evidence exists regarding long-term diet quality and the risk of type 2 diabetes among Asian populations, who have undergone a nutrition transition and a diabetes epidemic.
RESEARCH DESIGN AND METHODS - A total of 117,919 Chinese men and women, 40-74 years old, free of diabetes, cardiovascular disease, and cancer at baseline, were followed from 1996 to 2015. Diet quality was assessed by a healthy diet score (HDS) based on eight commonly consumed food groups previously suggested to be related to diabetes. Long-term diet quality and its changes were assessed by repeated surveys using food-frequency questionnaires.
RESULTS - We identified 6,111 incident diabetes cases during a mean follow-up of 11.5 years. Higher HDS was associated with lower diabetes risk (hazard ratio [HR] 0.85 [95% CI 0.78-0.92] in the highest vs. lowest quintile,<0.0001) after adjustment for potential confounders including BMI. Maintaining a high HDS during follow-up was associated with 26% lower risk compared with a consistently low HDS (HR 0.74 [95% CI 0.63-0.85]). The inverse association between HDS and diabetes was observed regardless of participants' age, sex, smoking and exercise habits, obesity status, and metabolic disease status but was more prominent among those who participated in leisure-time exercise (= 0.004). When considered jointly, a sustained high HDS plus exercise was associated with a 45% reduced risk of diabetes (HR 0.55 [95% CI 0.45-0.67]).
CONCLUSIONS - A high-quality diet, especially maintained over the long term and in conjunction with leisure-time exercise, is associated with lower risk of type 2 diabetes among urban Chinese adults.
© 2017 by the American Diabetes Association.
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Development of an eHealth Program for Parents of Adolescents With Type 1 Diabetes.
Whittemore R, Zincavage RM, Jaser SS, Grey M, Coleman JL, Collett D, Delvy R, Basile Ibrahim B, Marceau LD
(2018) Diabetes Educ 44: 72-82
Show Abstract · Added May 18, 2018
Purpose The purpose of this study was to understand the experience of parenting an adolescent with type 1 diabetes (T1DM), to develop a prototype of an eHealth program for parents of adolescents with T1DM, and to evaluate the prototype content and acceptability from the perspective of parents and health care providers. Methods A multiphase method was used generating both qualitative and quantitative data at multiple time points. There were 27 parents of adolescents aged 12 to 18 years with T1DM and 16 health care providers who participated in semistructured interviews to identify parental challenges; 53 parents and 27 providers evaluated the prototype. Thematic content analysis was used to analyze interview transcripts, and descriptive statistics were used to summarize survey data. Results Challenges experienced by parents of adolescents with T1DM included understanding the developmental and hormonal changes of adolescence that affect diabetes care, feeling tension between adolescent independence and parent control, communicating without nagging or conflict, transferring diabetes care responsibility safely, dealing with feelings of stress and distress, and perceiving a lack of resources for T1DM care and insufficient personal time for self-care. In the prototype evaluation, both parents and providers found content to be relevant and provided feedback to guide the development of the full program. Conclusions Parents of adolescents with T1DM and providers expressed a need for parents to have more support in transitioning diabetes care from parent to adolescent. eHealth programs offer an ideal way to address these needs and ultimately can be linked to electronic medical records improving quality and efficiency of health care in this population.
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Glucocorticoids Reprogram β-Cell Signaling to Preserve Insulin Secretion.
Fine NHF, Doig CL, Elhassan YS, Vierra NC, Marchetti P, Bugliani M, Nano R, Piemonti L, Rutter GA, Jacobson DA, Lavery GG, Hodson DJ
(2018) Diabetes 67: 278-290
Show Abstract · Added December 6, 2017
Excessive glucocorticoid exposure has been shown to be deleterious for pancreatic β-cell function and insulin release. However, glucocorticoids at physiological levels are essential for many homeostatic processes, including glycemic control. We show that corticosterone and cortisol and their less active precursors 11-dehydrocorticosterone (11-DHC) and cortisone suppress voltage-dependent Cachannel function and Cafluxes in rodent as well as in human β-cells. However, insulin secretion, maximal ATP/ADP responses to glucose, and β-cell identity were all unaffected. Further examination revealed the upregulation of parallel amplifying cAMP signals and an increase in the number of membrane-docked insulin secretory granules. Effects of 11-DHC could be prevented by lipotoxicity and were associated with paracrine regulation of glucocorticoid activity because global deletion of 11β-hydroxysteroid dehydrogenase type 1 normalized Caand cAMP responses. Thus, we have identified an enzymatically amplified feedback loop whereby glucocorticoids boost cAMP to maintain insulin secretion in the face of perturbed ionic signals. Failure of this protective mechanism may contribute to diabetes in states of glucocorticoid excess, such as Cushing syndrome, which are associated with frank dyslipidemia.
© 2017 by the American Diabetes Association.
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Shared Genetic Control of Brain Activity During Sleep and Insulin Secretion: A Laboratory-Based Family Study.
Morselli LL, Gamazon ER, Tasali E, Cox NJ, Van Cauter E, Davis LK
(2018) Diabetes 67: 155-164
MeSH Terms: Adiposity, Adult, Blood Glucose, Brain, Electroencephalography, Female, Glucose Tolerance Test, Humans, Insulin, Male, Middle Aged, Pedigree, Sleep
Show Abstract · Added November 29, 2017
Over the past 20 years, a large body of experimental and epidemiologic evidence has linked sleep duration and quality to glucose homeostasis, although the mechanistic pathways remain unclear. The aim of the current study was to determine whether genetic variation influencing both sleep and glucose regulation could underlie their functional relationship. We hypothesized that the genetic regulation of electroencephalographic (EEG) activity during non-rapid eye movement sleep, a highly heritable trait with fingerprint reproducibility, is correlated with the genetic control of metabolic traits including insulin sensitivity and β-cell function. We tested our hypotheses through univariate and bivariate heritability analyses in a three-generation pedigree with in-depth phenotyping of both sleep EEG and metabolic traits in 48 family members. Our analyses accounted for age, sex, adiposity, and the use of psychoactive medications. In univariate analyses, we found significant heritability for measures of fasting insulin sensitivity and β-cell function, for time spent in slow-wave sleep, and for EEG spectral power in the delta, theta, and sigma ranges. Bivariate heritability analyses provided the first evidence for a shared genetic control of brain activity during deep sleep and fasting insulin secretion rate.
© 2017 by the American Diabetes Association.
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13 MeSH Terms
Timing of Meal Insulin and Its Relation to Adherence to Therapy in Type 1 Diabetes.
Datye KA, Boyle CT, Simmons J, Moore DJ, Jaser SS, Sheanon N, Kittelsrud JM, Woerner SE, Miller KM, T1D Exchange
(2018) J Diabetes Sci Technol 12: 349-355
Show Abstract · Added September 13, 2017
The purpose of this study is to examine timing of meal insulin and further determine whether an association exists between timing of meal insulin and missed meal insulin doses. The cohort included 4768 T1D Exchange clinic registry participants <26 years with type 1 diabetes ≥1 year. Chi-square tests, t-tests, and regression were used to assess the relationship between participant characteristics and timing of meal insulin and missed meal doses, respectively. Timing of meal insulin and association with missed meal doses was analyzed using logistic regression. In all, 21% reported administering insulin several minutes before, 44% immediately before, 10% during, and 24% after meal. Participants who gave insulin prior to a meal had significantly lower HbA1c than those who gave insulin during or after meal (8.4% ± 1.5% vs 8.8% ± 1.6%, adjusted P < .001), but no significant association was observed regarding DKA events. Those who reported missing ≥1 insulin dose per week had higher HbA1c (9.8% ± 1.9% vs 8.3% ± 1.3%, adjusted P < .001) and were more likely to experience at least one DKA event (9% vs 5%, adjusted P = .001) compared with those who rarely missed a meal insulin dose. Participants who reported administering insulin during or after a meal were more likely to report missing ≥1 meal insulin dose per week compared with those who administered insulin before a meal (28% vs 14%, adjusted P < .001). Premeal insulin was associated with lower HbA1c and fewer missed meal insulin doses. Providers may use this information to discuss the benefits of premeal insulin on glycemic control and adherence to therapy.
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Defining a Novel Role for the Pdx1 Transcription Factor in Islet β-Cell Maturation and Proliferation During Weaning.
Spaeth JM, Gupte M, Perelis M, Yang YP, Cyphert H, Guo S, Liu JH, Guo M, Bass J, Magnuson MA, Wright C, Stein R
(2017) Diabetes 66: 2830-2839
MeSH Terms: Animals, Cell Proliferation, Gene Expression Regulation, Homeodomain Proteins, Insulin-Secreting Cells, Male, Mice, Mice, Knockout, Oxidative Phosphorylation, Trans-Activators, Weaning
Show Abstract · Added August 1, 2017
The transcription factor encoded by thegene is a critical transcriptional regulator, as it has fundamental actions in the formation of all pancreatic cell types, islet β-cell development, and adult islet β-cell function. Transgenic- and cell line-based experiments have identified 5'-flanking conserved sequences that control pancreatic and β-cell type-specific transcription, which are found within areas I (bp -2694 to -2561), II (bp -2139 to -1958), III (bp -1879 to -1799), and IV (bp -6200 to -5670). Because of the presence in area IV of binding sites for transcription factors associated with pancreas development and islet cell function, we analyzed how an endogenous deletion mutant affectedexpression embryonically and postnatally. The most striking result was observed in malemutant mice after 3 weeks of birth (i.e., the onset of weaning), with only a small effect on pancreas organogenesis and no deficiencies in their female counterparts. Compromised Pdx1 mRNA and protein levels in weaned male mutant β-cells were tightly linked with hyperglycemia, decreased β-cell proliferation, reduced β-cell area, and altered expression of Pdx1-bound genes that are important in β-cell replication, endoplasmic reticulum function, and mitochondrial activity. We discuss the impact of these novel findings togene regulation and islet β-cell maturation postnatally.
© 2017 by the American Diabetes Association.
2 Communities
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11 MeSH Terms
Chronic β-Cell Depolarization Impairs β-Cell Identity by Disrupting a Network of Ca-Regulated Genes.
Stancill JS, Cartailler JP, Clayton HW, O'Connor JT, Dickerson MT, Dadi PK, Osipovich AB, Jacobson DA, Magnuson MA
(2017) Diabetes 66: 2175-2187
MeSH Terms: Animals, Basic Helix-Loop-Helix Transcription Factors, Calcium, Calcium Signaling, Cell Adhesion, Cell Cycle Proteins, Cell Lineage, Cell Polarity, Gene Expression, Gene Expression Regulation, Insulin-Secreting Cells, KATP Channels, Mice, Pancreatic Polypeptide-Secreting Cells, S100 Calcium Binding Protein A6, S100 Calcium-Binding Protein A4, S100 Proteins, Sulfonylurea Receptors
Show Abstract · Added June 2, 2017
We used mice lacking, a key component of the β-cell K-channel, to analyze the effects of a sustained elevation in the intracellular Caconcentration ([Ca]) on β-cell identity and gene expression. Lineage tracing analysis revealed the conversion of β-cells lackinginto pancreatic polypeptide cells but not to α- or δ-cells. RNA-sequencing analysis of FACS-purifiedβ-cells confirmed an increase ingene expression and revealed altered expression of more than 4,200 genes, many of which are involved in Casignaling, the maintenance of β-cell identity, and cell adhesion. The expression ofand, two highly upregulated genes, is closely correlated with membrane depolarization, suggesting their use as markers for an increase in [Ca]Moreover, a bioinformatics analysis predicts that many of the dysregulated genes are regulated by common transcription factors, one of which,, was confirmed to be directly controlled by Cainflux in β-cells. Interestingly, among the upregulated genes is, a putative marker of β-cell dedifferentiation, and other genes associated with β-cell failure. Taken together, our results suggest that chronically elevated β-cell [Ca]inislets contributes to the alteration of β-cell identity, islet cell numbers and morphology, and gene expression by disrupting a network of Ca-regulated genes.
© 2017 by the American Diabetes Association.
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18 MeSH Terms