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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
MeSH Terms: Adolescent, Adolescent Behavior, Blood Glucose, Blood Glucose Self-Monitoring, Caregivers, Cross-Sectional Studies, Diabetes Mellitus, Type 1, Female, Glycated Hemoglobin A, Humans, Hyperglycemia, Hypoglycemia, Hypoglycemic Agents, Insulin, Insulin Infusion Systems, Male, Patient Compliance, Self Report, Self-Management, Tennessee
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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20 MeSH Terms
Sleep in Type 1 Diabetes: Implications for Glycemic Control and Diabetes Management.
Perez KM, Hamburger ER, Lyttle M, Williams R, Bergner E, Kahanda S, Cobry E, Jaser SS
(2018) Curr Diab Rep 18: 5
MeSH Terms: Diabetes Mellitus, Type 1, Humans, Hyperglycemia, Patient Compliance, Sleep, Sleep Wake Disorders, Treatment Outcome
Show Abstract · Added May 15, 2018
PURPOSE OF REVIEW - To highlight recent findings from studies of sleep in type 1 diabetes (T1D), with a focus on the role of sleep in self-management, the cognitive and psychosocial outcomes related to sleep disturbances, and factors associated with sleep disturbances specific to T1D.
RECENT FINDINGS - People with T1D experience higher rates of sleep disturbances than people without diabetes, and these disturbances have negative implications for glycemic control and diabetes management, as well as psychosocial and cognitive outcomes. Inconsistent sleep timing (bedtime and wake time) has emerged as a potential target for interventions, as variability in sleep timing has been linked with poorer glycemic control and adherence to treatment. Sleep-promoting interventions and new diabetes technology have the potential to improve sleep in people with T1D. Sleep is increasingly considered a critical factor in diabetes management, but more multi-method and longitudinal research is needed. We emphasize the importance of sufficient and consistent sleep for people with T1D, and the need for providers to routinely assess sleep among patients with T1D.
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3 Members
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7 MeSH Terms
Central injection of fibroblast growth factor 1 induces sustained remission of diabetic hyperglycemia in rodents.
Scarlett JM, Rojas JM, Matsen ME, Kaiyala KJ, Stefanovski D, Bergman RN, Nguyen HT, Dorfman MD, Lantier L, Wasserman DH, Mirzadeh Z, Unterman TG, Morton GJ, Schwartz MW
(2016) Nat Med 22: 800-6
MeSH Terms: Adipose Tissue, Animals, Blood Glucose, Blotting, Western, Body Composition, Brain, Carbon Radioisotopes, Deoxyglucose, Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 2, Diet, High-Fat, Disease Models, Animal, Ependymoglial Cells, Fibroblast Growth Factor 1, Forkhead Box Protein O1, Glucose Tolerance Test, Heart, Heat-Shock Proteins, Hyperglycemia, Hypothalamus, Injections, Intraventricular, Liver, Male, Mice, Mice, Knockout, Mice, Obese, Muscle, Skeletal, Myocardium, Neoplasm Proteins, Proto-Oncogene Proteins c-fos, Rats, Rats, Zucker, Real-Time Polymerase Chain Reaction, Receptor, Insulin, Remission Induction
Show Abstract · Added May 16, 2019
Type 2 diabetes (T2D) is among the most common and costly disorders worldwide. The goal of current medical management for T2D is to transiently ameliorate hyperglycemia through daily dosing of one or more antidiabetic drugs. Hypoglycemia and weight gain are common side effects of therapy, and sustained disease remission is not obtainable with nonsurgical approaches. On the basis of the potent glucose-lowering response elicited by activation of brain fibroblast growth factor (FGF) receptors, we explored the antidiabetic efficacy of centrally administered FGF1, which, unlike other FGF peptides, activates all FGF receptor subtypes. We report that a single intracerebroventricular injection of FGF1 at a dose one-tenth of that needed for antidiabetic efficacy following peripheral injection induces sustained diabetes remission in both mouse and rat models of T2D. This antidiabetic effect is not secondary to weight loss, does not increase the risk of hypoglycemia, and involves a novel and incompletely understood mechanism for increasing glucose clearance from the bloodstream. We conclude that the brain has an inherent potential to induce diabetes remission and that brain FGF receptors are potential pharmacological targets for achieving this goal.
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MeSH Terms
Hyperglycemic clamp-derived disposition index is negatively associated with metabolic syndrome severity in obese subjects.
Shah SS, Ramirez CE, Powers AC, Yu C, Shibao CA, Luther JM
(2016) Metabolism 65: 835-42
MeSH Terms: Adult, Age Factors, Blood Glucose, Female, Glucose Tolerance Test, Humans, Hyperglycemia, Insulin, Insulin Secretion, Male, Metabolic Syndrome, Middle Aged, Obesity, Severity of Illness Index, Sex Factors, Waist Circumference
Show Abstract · Added July 16, 2016
OBJECTIVE - Metabolic syndrome is associated with insulin resistance and increased future risk of type 2 diabetes. This study investigates the relationship between insulin secretion, insulin resistance and individual metabolic syndrome components in subjects without a prior diagnosis of diabetes.
RESEARCH DESIGN AND METHODS - We assessed insulin secretion during hyperglycemic clamps by infusing dextrose to maintain hyperglycemia (200mg/dL), followed by L-arginine administration. Studies in 98 individuals (mean age 45.3±1.2years, 56% female, 22% African-American, 49% with metabolic syndrome) were analyzed. We tested the association between the number of metabolic syndrome components and individual outcome variables using linear mixed-effects models to adjust for potential confounding effects of age, sex, and race.
RESULTS - Insulin sensitivity index was reduced in the presence of 1 or more metabolic syndrome components. Insulin sensitivity was independently associated with age, waist circumference, male gender and decreased HDL cholesterol. The acute insulin response was greater with two or more metabolic syndrome components, and late glucose-stimulated and L-arginine-stimulated insulin responses exhibited a similar trend. In contrast, the disposition index, a measure of beta cell compensation for insulin resistance, was linearly lower with the number of metabolic syndrome components, and was negatively associated with age, Caucasian race, waist circumference, fasting glucose, and decreased HDL cholesterol.
CONCLUSIONS - The insulin secretory response in metabolic syndrome is inadequate for the worsening insulin sensitivity, as demonstrated by a decline in disposition index. A dysfunctional insulin secretory response is evident in non-diabetic individuals and worsens with accumulation of metabolic syndrome components.
Copyright © 2016 Elsevier Inc. All rights reserved.
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16 MeSH Terms
How do I manage hyperglycemia/post-transplant diabetes mellitus after allogeneic HSCT.
Fuji S, Rovó A, Ohashi K, Griffith M, Einsele H, Kapp M, Mohty M, Majhail NS, Engelhardt BG, Tichelli A, Savani BN
(2016) Bone Marrow Transplant 51: 1041-9
MeSH Terms: Diabetes Mellitus, Disease Management, Forecasting, Hematopoietic Stem Cell Transplantation, Humans, Hyperglycemia, Transplantation, Homologous
Show Abstract · Added July 28, 2016
Allogeneic hematopoietic stem cell transplantation (allo-HSCT) recipients frequently develop glucose intolerance and post-transplant diabetes mellitus (PTDM). The clinical importance of PTDM and its detrimental impact on HSCT outcomes are under-recognized. After allo-HSCT, various mechanisms can contribute to the development of PTDM. Here we review information about hyperglycemia and PTDM after allo-HSCT as well as PTDM after solid organ transplantation and describe ways to manage hyperglycemia/PTDM after allogeneic HSCT. Taking into consideration a lack of well-established evidence in the field of allo-HSCT, more studies should be conducted in the future, which will require closer multidisciplinary collaboration between hematologists, endocrinologists and nutritionists.
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7 MeSH Terms
Lack of Prox1 Downregulation Disrupts the Expansion and Maturation of Postnatal Murine β-Cells.
Paul L, Walker EM, Drosos Y, Cyphert HA, Neale G, Stein R, South J, Grosveld G, Herrera PL, Sosa-Pineda B
(2016) Diabetes 65: 687-98
MeSH Terms: Animals, Animals, Newborn, Cell Differentiation, Cell Line, Cell Proliferation, Chromatin Immunoprecipitation, Computer Simulation, Down-Regulation, Enzyme-Linked Immunosorbent Assay, Gene Expression Profiling, Gene Knockdown Techniques, Glucose Tolerance Test, Homeodomain Proteins, Humans, Hyperglycemia, Insulin, Insulin-Secreting Cells, Maf Transcription Factors, Large, Mice, Mice, Transgenic, RNA, Messenger, Real-Time Polymerase Chain Reaction, Tumor Suppressor Proteins
Show Abstract · Added September 19, 2016
Transcription factor expression fluctuates during β-cell ontogeny, and disruptions in this pattern can affect the development or function of those cells. Here we uncovered that murine endocrine pancreatic progenitors express high levels of the homeodomain transcription factor Prox1, whereas both immature and mature β-cells scarcely express this protein. We also investigated if sustained Prox1 expression is incompatible with β-cell development or maintenance using transgenic mouse approaches. We discovered that Prox1 upregulation in mature β-cells has no functional consequences; in contrast, Prox1 overexpression in immature β-cells promotes acute fasting hyperglycemia. Using a combination of immunostaining and quantitative and comparative gene expression analyses, we determined that Prox1 upregulation reduces proliferation, impairs maturation, and enables apoptosis in postnatal β-cells. Also, we uncovered substantial deficiency in β-cells that overexpress Prox1 of the key regulator of β-cell maturation MafA, several MafA downstream targets required for glucose-stimulated insulin secretion, and genes encoding important components of FGF signaling. Moreover, knocking down PROX1 in human EndoC-βH1 β-cells caused increased expression of many of these same gene products. These and other results in our study indicate that reducing the expression of Prox1 is beneficial for the expansion and maturation of postnatal β-cells.
© 2016 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
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23 MeSH Terms
The gastrin-releasing peptide analog bombesin preserves exocrine and endocrine pancreas morphology and function during parenteral nutrition.
Pierre JF, Neuman JC, Brill AL, Brar HK, Thompson MF, Cadena MT, Connors KM, Busch RA, Heneghan AF, Cham CM, Jones EK, Kibbe CR, Davis DB, Groblewski GE, Kudsk KA, Kimple ME
(2015) Am J Physiol Gastrointest Liver Physiol 309: G431-42
MeSH Terms: Amylases, Animals, Bombesin, DNA, Food, Formulated, Gastrin-Releasing Peptide, Gene Expression Regulation, Hyperglycemia, Islets of Langerhans, Lipase, Male, Mice, Mice, Inbred ICR, Pancreas, Exocrine, Pancreatic Hormones, Parenteral Nutrition
Show Abstract · Added August 2, 2016
Stimulation of digestive organs by enteric peptides is lost during total parental nutrition (PN). Here we examine the role of the enteric peptide bombesin (BBS) in stimulation of the exocrine and endocrine pancreas during PN. BBS protects against exocrine pancreas atrophy and dysfunction caused by PN. BBS also augments circulating insulin levels, suggesting an endocrine pancreas phenotype. While no significant changes in gross endocrine pancreas morphology were observed, pancreatic islets isolated from BBS-treated PN mice showed a significantly enhanced insulin secretion response to the glucagon-like peptide-1 (GLP-1) agonist exendin-4, correlating with enhanced GLP-1 receptor expression. BBS itself had no effect on islet function, as reflected in low expression of BBS receptors in islet samples. Intestinal BBS receptor expression was enhanced in PN with BBS, and circulating active GLP-1 levels were significantly enhanced in BBS-treated PN mice. We hypothesized that BBS preserved islet function indirectly, through the enteroendocrine cell-pancreas axis. We confirmed the ability of BBS to directly stimulate intestinal enteroid cells to express the GLP-1 precursor preproglucagon. In conclusion, BBS preserves the exocrine and endocrine pancreas functions during PN; however, the endocrine stimulation is likely indirect, through the enteroendocrine cell-pancreas axis.
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16 MeSH Terms
Phenotypic Characterization of MIP-CreERT1Lphi Mice With Transgene-Driven Islet Expression of Human Growth Hormone.
Oropeza D, Jouvet N, Budry L, Campbell JE, Bouyakdan K, Lacombe J, Perron G, Bergeron V, Neuman JC, Brar HK, Fenske RJ, Meunier C, Sczelecki S, Kimple ME, Drucker DJ, Screaton RA, Poitout V, Ferron M, Alquier T, Estall JL
(2015) Diabetes 64: 3798-807
MeSH Terms: Animals, Blood Glucose, Diabetes Mellitus, Experimental, Homeostasis, Human Growth Hormone, Humans, Hyperglycemia, Insulin, Insulin-Secreting Cells, Male, Mice, Mice, Transgenic, Phenotype
Show Abstract · Added August 2, 2016
There is growing concern over confounding artifacts associated with β-cell-specific Cre-recombinase transgenic models, raising questions about their general usefulness in research. The inducible β-cell-specific transgenic (MIP-CreERT(1Lphi)) mouse was designed to circumvent many of these issues, and we investigated whether this tool effectively addressed concerns of ectopic expression and disruption of glucose metabolism. Recombinase activity was absent from the central nervous system using a reporter line and high-resolution microscopy. Despite increased pancreatic insulin content, MIP-CreERT mice on a chow diet exhibited normal ambient glycemia, glucose tolerance and insulin sensitivity, and appropriate insulin secretion in response to glucose in vivo and in vitro. However, MIP-CreERT mice on different genetic backgrounds were protected from high-fat/ streptozotocin (STZ)-induced hyperglycemia that was accompanied by increased insulin content and islet density. Ectopic human growth hormone (hGH) was highly expressed in MIP-CreERT islets independent of tamoxifen administration. Circulating insulin levels remained similar to wild-type controls, whereas STZ-associated increases in α-cell number and serum glucagon were significantly blunted in MIP-CreERT(1Lphi) mice, possibly due to paracrine effects of hGH-induced serotonin expression. These studies reveal important new insight into the strengths and limitations of the MIP-CreERT mouse line for β-cell research.
© 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
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1 Members
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13 MeSH Terms
Acute effects of hyperinsulinemia and hyperglycemia on vascular inflammatory biomarkers and endothelial function in overweight and obese humans.
Perkins JM, Joy NG, Tate DB, Davis SN
(2015) Am J Physiol Endocrinol Metab 309: E168-76
MeSH Terms: Adult, Biomarkers, Blood Glucose, Endothelium, Vascular, Female, Glucose Clamp Technique, Humans, Hyperglycemia, Hyperinsulinism, Inflammation Mediators, Insulin, Male, Obesity, Overweight, Vasculitis
Show Abstract · Added July 30, 2015
We investigated the separate and combined effects of hyperglycemia and hyperinsulinemia on markers of endothelial function, proinflammatory and proatherothrombotic responses in overweight/obese nondiabetic humans. Twenty-two individuals (13 F/9 M, BMI 30.1 ± 4.1 kg/m(2)) were studied during four randomized, single-blind protocols. The pancreatic clamp technique was combined with 4-h glucose clamps consisting of either 1) euinsulinemia-euglycemia, 2) euinsulinemia-hyperglycemia, 3) hyperinsulinemia-hyperglycemia, or 4) hyperinsulinemia-euglycemia. Insulin levels were higher (998 ± 66 vs. 194 ± 22 pmol/l) during hyperinsulinemia compared with euinsulinemia. Glucose levels were 11.1 mmol/l during hyperinsulinemia compared with 5.1 ± 0.1 mmol/l during euglycemia. VCAM, ICAM, P-selectin, E-selectin, IL-6, adiponectin, and PAI-1 responses were all increased (P < 0.01-0.0001), and endothelial function was decreased (P < 0.0005) during euinsulinemia-hyperglycemia compared with other protocols. Hyperinsulinemia in the presence of hyperglycemia prevented the increase in proinflammatory and proatherothrombotic markers while also normalizing vascular endothelial function. We conclude that 4 h of moderate hyperglycemia can result in increases of proinflammatory markers (ICAM, VCAM, IL-6, E-selectin), platelet activation (P-selectin), reduced fibrinolytic balance (increased PAI-1), and disordered endothelial function in a group of obese and overweight individuals. Hyperinsulinemia prevents the actions of moderate hyperglycemia to reduce endothelial function and increase proinflammatory and proatherothrombotic markers.
Copyright © 2015 the American Physiological Society.
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15 MeSH Terms
Glypican-5 Increases Susceptibility to Nephrotic Damage in Diabetic Kidney.
Okamoto K, Honda K, Doi K, Ishizu T, Katagiri D, Wada T, Tomita K, Ohtake T, Kaneko T, Kobayashi S, Nangaku M, Tokunaga K, Noiri E
(2015) Am J Pathol 185: 1889-98
MeSH Terms: Adult, Aged, Animals, Cell Line, Diabetes Mellitus, Type 2, Diabetic Nephropathies, Disease Susceptibility, Female, Fibroblast Growth Factor 2, Glomerular Mesangium, Glypicans, Humans, Hyperglycemia, Kidney, Kidney Failure, Chronic, Male, Mesangial Cells, Mice, Mice, Inbred C57BL, Mice, Knockout, Middle Aged, Nephrotic Syndrome, Podocytes, Proteinuria, Rats
Show Abstract · Added February 11, 2016
Type 2 diabetes mellitus is a leading health issue worldwide. Among cases of diabetes mellitus nephropathy (DN), the major complication of type 2 diabetes mellitus, the nephrotic phenotype is often intractable to clinical intervention and demonstrates the rapid decline of renal function to end-stage renal disease. We recently identified the gene for glypican-5 (GPC5), a cell-surface heparan sulfate proteoglycan, as conferring susceptibility for acquired nephrotic syndrome and additionally identified an association through a genome-wide association study between a variant in GPC5 and DN of type 2 diabetes mellitus. In vivo and in vitro data showed a progressive increase of GPC5 in type 2 DN along with severity; the excess was derived from glomerular mesangial cells. In this study, diabetic kidney showed that accumulation of fibroblast growth factor (Fgf)2 strikingly induced progressive proteinuria that was avoided in Gpc5 knockdown mice. The efficacy of Gpc5 inhibition was exerted through expression of the Fgf receptors 3 and 4 provoked in the diabetic kidney attributively. Extraglomerular Fgf2 was pathogenic in DN, and the deterrence of Gpc5 effectively inhibited the glomerular accumulation of Fgf2, the subsequent increase of mesangial extracellular matrix, and the podocytes' small GTPase activity. These findings elucidate the pivotal role of GPC5, identified as a susceptible gene in the genome-wide association study, in hyperglycemia-induced glomerulopathy.
Copyright © 2015 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
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25 MeSH Terms