Instituting a Successful Discharge Plan for Patients With Type 2 Diabetes: Challenges and Solutions.

Achieving target inpatient glycemic management outcomes has been shown to influence important clinical outcomes such as hospital length of stay and readmission rates. However, arguably the most profound, lasting impact of inpatient diabetes management is achieved at the time of discharge-namely reconciling and prescribing the right medications and making referrals for follow-up. Discharge planning offers a unique opportunity to break through therapeutic inertia, offer diabetes self-management education, and institute an individualized treatment plan that prepares the patient for discharge and promotes self-care and engagement. However, the path to a successful discharge plan can be fraught with potential pitfalls for clinicians, including lack of knowledge and experience with newer diabetes medications, costs, concerns over insurance coverage, and lack of time and resources. This article presents an algorithm to assist clinicians in selecting discharge regimens that maximize benefits and reduce barriers to self-care for patients and a framework for creating an interdisciplinary hospital diabetes discharge program.

Colchicine's effects on metabolic and inflammatory molecules in adults with obesity and metabolic syndrome: results from a pilot randomized controlled trial.

OBJECTIVE: Recent clinical trials have demonstrated that colchicine may have metabolic and cardiovascular and benefits in at-risk patients; however, the mechanisms through which colchicine may improve outcomes are still unclear. We sought to examine colchicine's effects on circulating inflammatory and metabolic molecules in adults with obesity and metabolic syndrome (MetS). METHODS: Blood samples were collected pre- and post-intervention during a double-blind randomized controlled trial in which 40 adults with obesity and MetS were randomized to colchicine 0.6 mg or placebo twice-daily for 3 months. Serum samples were analyzed for 1305 circulating factors using the SomaScan Platform. The Benjamini-Hochberg procedure was used to adjust the false discovery rate (FDR) for multiple testing. RESULTS: At baseline, age (48.0 ± 13.8 vs. 44.7 ± 10.3 years) and BMI (39.8 ± 6.4 vs. 41.8 ± 8.2 kg/m2) were not different between groups. After controlling for the FDR, 34 molecules were significantly changed by colchicine. Colchicine decreased concentrations of multiple inflammatory molecules, including C-reactive protein, interleukin 6, and resistin, in addition to vascular-related proteins (e.g., oxidized low-density lipoprotein receptor, phosphodiesterase 5A). Conversely, relative to placebo, colchicine significantly increased concentrations of eight molecules including secreted factors associated with metabolism and anti-thrombosis. CONCLUSIONS: In adults with obesity, colchicine significantly affected concentrations of proteins involved in the innate immune system, endothelial function and atherosclerosis, uncovering new mechanisms behind its cardiometabolic effects. Further research is warranted to investigate whether colchicine's IL-6 suppressive effects may be beneficial in COVID-19.

Bacitracin attenuates haemolysis-induced insulin degradation during insulin sensitivity testing: Repurposing an old drug for use in metabolic research.

Haemolysis of serially collected insulin serum samples frequently causes falsely-low measured concentrations because of the release of intracellular insulin degrading enzyme (IDE). We investigated if bacitracin, an in vitro IDE inhibitor, could prevent haemolysis-induced insulin degradation during insulin sensitivity testing. Blood samples were collected from adults undergoing serial sampling for insulin sensitivity. A dose-finding study measured insulin from experimentally haemolysed samples containing five bacitracin concentrations (0-2.5 g/L) and from non-experimentally haemolysed samples. To confirm the utility of bacitracin in the clinical setting, we compared insulin in samples collected with and without 1 g/L bacitracin from a frequently sampled intravenous glucose tolerance test (FSIVGTT), where haemolysis often occurs accidentally. In the dose-finding study, bacitracin 0.25, 1 and 2.5 g/L all maximally prevented insulin degradation in experimentally haemolysed samples. Among FSIVGTT unintentionally haemolysed samples, insulin concentrations from bacitracin-containing samples were significantly higher than from those without bacitracin (P < .01), and not different from non-haemolysed samples obtained simultaneously from a second intravenous catheter (P = .07). Bacitracin did not significantly alter insulin concentrations in non-haemolysed samples. Bacitracin attenuates haemolysis-associated insulin degradation in clinical samples, enabling a more accurate assessment of insulin sensitivity and glucose homeostasis.

Depressive symptoms in adolescent girls at-risk for type 2 diabetes and their parents.

Few studies have characterized the relation between parent's depression symptoms and adolescent's depression symptoms in adolescents at-risk for type 2 diabetes (T2D). We evaluated the associations of parental depression symptoms with the depression symptoms and metabolic functioning of adolescent offspring at-risk for T2D. One-hundred sixteen parents and adolescent girls with a family history of diabetes completed surveys of depression symptoms. Adolescents' degree of metabolic risk for T2D was estimated from body mass index (BMI; kg/m2) standard score, percent adiposity from dual-energy x-ray absorptiometry scan, and whole body insulin sensitivity index determined from glucose/insulin concentrations during a two-hour oral glucose tolerance test. Parents' and adolescents' depression symptoms were significantly associated, even after accounting for race/ethnicity, age, puberty, body composition, and parental diabetes/BMI. Adjusting for similar covariates, parent depression symptoms also were positively related to adolescents' BMI standard score and had a trend-level association with adiposity. There was an inverse relation between parental depression symptoms and adolescent insulin sensitivity, which was entirely accounted for by adolescent body composition. The associations of parental depression symptoms with more elevated depression symptoms and higher BMI in adolescents at-risk for T2D has potential implications for interventions addressing these co-morbid health conditions.

Subcutaneous adipose tissue imaging of human obesity reveals two types of adipocyte membranes: Insulin-responsive and -nonresponsive.

In adipose tissue, resistance to insulin's ability to increase glucose uptake can be induced by multiple factors, including obesity. Impaired insulin action may take place at different spatial loci at the cellular or subcellular level. To begin to understand the spatial response to insulin in human subcutaneous adipose tissue (hSAT), we developed a quantitative imaging method for activation of a major signaling node in the glucoregulatory insulin signaling pathway. After treatment with insulin or control media, biopsied tissues were immunostained for Akt phosphorylation at Thr-308/9 (pAkt) and then imaged by confocal fluorescence microscopy automated to collect a large grid of high resolution fields. In hSAT from 40 men and women with obesity, substantial heterogeneity of pAkt densities in adipocyte membranes were quantified in each image mosaic using a spatial unit of at least twice the size of the point spread function. Statistical analysis of the distribution of pAkt spatial units was best fit as the weighted sum of two separate distributions, corresponding to either a low or high pAkt density. A "high pAkt fraction" metric was calculated from the fraction of high pAkt distributed units over the total units. Importantly, upon insulin stimulation, tissues from the same biopsy showed either a minimal or a substantial change in the high pAkt fraction. Further supporting a two-state response to insulin stimulation, subjects with similar insulin sensitivity indices are also segregated into either of two clusters identified by the amount of membrane-localized pAkt.

Associations of the melanocortin 3 receptor C17A + G241A haplotype with body composition and inflammation in African-American adults.

BACKGROUND: The MC3R haplotype C17A + G241A, which encodes a partially inactivated receptor, has high prevalence in individuals of predominately African ancestry. In pediatric cohorts, homozygosity for this common variant has been associated with obesity, reduced lean mass, and greater fasting insulin. However, metabolic and body composition measures have not been well studied in adults with this haplotype. METHODS: A convenience sample of 237 healthy African-American adult volunteers was studied. TaqMan assays were used to genotype MC3R variants. Labs were drawn in the morning in the fasted state. Body composition data was obtained via dual-energy X-ray absorptiometry. An analysis of covariance was used to examine the associations of genotype with metabolic and body composition measures controlling for age and sex. RESULTS: Individuals homozygous for the MC3R C17A + G241A haplotype had significantly greater body mass index, fat mass, fat mass percentage, and C-reactive protein, with reduced lean mass percentage as compared to heterozygous and wild-type participants (all ps < 0.05); fasting insulin was marginally nonsignificant between groups (p = 0.053). After adjusting for fat mass, laboratory differences no longer remained significant. CONCLUSIONS: Homozygosity for MC3R C17A + G241A is associated with increased adiposity in African-American adults. Further studies are needed to elucidate the mechanisms behind these associations.

Effects of colchicine in adults with metabolic syndrome: A pilot randomized controlled trial.

AIM: To evaluate the efficacy and safety of colchicine for improving metabolic and inflammatory outcomes in people with obesity and metabolic syndrome (MetS). MATERIALS AND METHODS: Adults with obesity and MetS, but who did not have diabetes, were randomized to colchicine 0.6 mg or placebo capsules twice daily for 3 months. The primary outcome was change in insulin sensitivity (SI ) as estimated by insulin-modified frequently sampled intravenous glucose tolerance tests. Secondary outcomes included changes in other metabolic variables and inflammatory markers. RESULTS: Of 40 participants randomized (21 colchicine, 19 placebo), 37 completed the trial. Compared with placebo, colchicine significantly reduced C-reactive protein (P <0.005), erythrocyte sedimentation rate (P <0.01), white blood cell count (P <0.005), and absolute neutrophil count (P <0.001). Change in SI was not significantly different between colchicine and placebo arms (difference: +0.21 × 10-5 ; CI -1.70 to +2.13 × 10-5 min-1 mU-1 mL; P = 0.82). However, changes in some secondary outcomes, including homeostatic model assessment of insulin resistance (P = 0.0499), fasting insulin (P = 0.07) and glucose effectiveness (P = 0.08), suggested metabolic improvements in the colchicine versus placebo group. Adverse events were generally mild and similar in both groups. CONCLUSIONS: This pilot study found colchicine significantly improved obesity-associated inflammatory variables and showed a good safety profile among adults with obesity and MetS who did not have diabetes. These results suggest a larger, adequately powered study should be conducted to determine whether colchicine improves insulin resistance and other measures of metabolic health in at-risk individuals.

Pediatric Loss-of-Control Eating and Anxiety in Relation to Components of Metabolic Syndrome.

Objective: Pediatric loss-of-control (LOC) eating is associated with, and predictive of, gains in adiposity and adverse metabolic outcomes. In addition, some preliminary data suggest that anxiety may exacerbate the relationship of LOC eating with weight and metabolic syndrome (MetS)-related measures. We therefore examined whether anxiety moderated the relationship between LOC eating and body mass index z (BMIz), adiposity, and MetS-related measures in youth. Methods: A convenience sample of non-treatment-seeking boys and girls of varying weight strata were interviewed to determine the presence of LOC eating and completed a questionnaire assessing trait anxiety. BMIz and MetS-related measures (blood pressure, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, glucose, and insulin) were measured after an overnight fast. Adiposity was assessed by air displacement plethysmography or dual-energy x-ray absorptiometry. Analyses adjusted for age, sex, race, height, fat mass, and depressive symptoms, as appropriate. Results: In all, 379 youths (13.0 ± 2.8 years; 53% female; BMIz = 0.8 ± 1.1; 22% with LOC eating) were studied. Anxiety was not significantly related to BMIz, adiposity, or MetS-related measures. However, anxiety and LOC eating interacted such that only among youth with LOC eating, anxiety was positively associated with fasting insulin (p = .02) and insulin resistance (p = .01). The interaction of anxiety and LOC eating was not significantly related to BMIz, adiposity, or any other MetS-related measure (ps = ns). Conclusions: Only among non-treatment-seeking youth with LOC eating, anxiety may be associated with increased insulin secretion and insulin resistance. Longitudinal studies are required to confirm these findings and explore mechanisms for these relationships.

Successful Treatment of Estrogen Excess in Primary Bilateral Macronodular Adrenocortical Hyperplasia with Leuprolide Acetate.

Primary bilateral macronodular adrenocortical hyperplasia (PBMAH) is an uncommon cause of adrenal Cushing syndrome (CS) in which cortisol and occasionally other steroid hormones can be secreted under the influence of aberrantly expressed G-protein coupled receptors (GPCRs) in the adrenal cortex. We describe the unique case of a 64-year-old postmenopausal female with PBMAH whose adrenal lesions expressed luteinizing hormone receptors (LHr). She presented initially with CS and underwent right adrenalectomy; a few years later she presented with macromastia and mastodynia, possibly due to estrogen excess from her remaining left adrenocortical masses. Testing before and after treatment with quarterly leuprolide acetate therapy and immunohistochemistry on tissue and targeted sequencing of the genes of interest were performed. Tissue from the patient's right adrenal was tested for P450 aromatase (CYP19A1) and LHr expression; both were expressed throughout the hyperplastic cortex, although expression was more intense in the adenomatous areas. Targeted sequencing revealed a pathogenic PDE11A mutation, as well as variants in the ARMC5 and INHA genes. PDE11A expression was decreased in the adenoma but there was no loss of heterozygosity for the PDE11A locus. Because of the clinical presentation and LHr expression, quarterly leuprolide acetate therapy was started. Shortly after initiation of therapy, the patient reported decreased breast size and pain; she remains well controlled to date, after 10 years of treatment. This is the first description of a patient with PBMAH presenting with severe macromastia and mastodynia from what appears to be excess estrogen production from her adrenal tumor. The patient had a long-lasting response to chronic leuprolide acetate treatment, showing that drug therapy exploiting the aberrant receptor expression in PBMAH is possible even in the absence of cortisol overproduction.

Polymorphisms and mutations in the melanocortin-3 receptor and their relation to human obesity.

Inactivating mutations in the melanocortin 3 receptor (Mc3r) have been described as causing obesity in mice, but the physiologic effects of MC3R mutations in humans have been less clear. Here we review the MC3R polymorphisms and mutations identified in humans, and the in vitro, murine, and human cohort studies examining their putative effects. Some, but not all, studies suggest that the common human MC3R variant T6K+V81I, as well as several other rare, function-altering mutations, are associated with greater adiposity and hyperleptinemia with altered energy partitioning. In vitro, the T6K+V81I variant appears to decrease MC3R expression and therefore cAMP generation in response to ligand binding. Knockin mouse studies confirm that the T6K+V81I variant increases feeding efficiency and the avidity with which adipocytes derived from bone or adipose tissue stem cells store triglycerides. Other MC3R mutations occur too infrequently in the human population to make definitive conclusions regarding their clinical effects. This article is part of a Special Issue entitled: Melanocortin Receptors - edited by Ya-Xiong Tao.

Prevention of insulin resistance in adolescents at risk for type 2 diabetes with depressive symptoms: 1-year follow-up of a randomized trial.

BACKGROUND: Depression is associated with poor insulin sensitivity. We evaluated the long-term effects of a cognitive behavioral therapy (CBT) program for prevention of depression on insulin sensitivity in adolescents at risk for type 2 diabetes (T2D) with depressive symptoms. METHODS: One-hundred nineteen adolescent females with overweight/obesity, T2D family history, and mild-to-moderate depressive symptoms were randomized to a 6-week CBT group (n = 61) or 6-week health education (HE) control group (n = 58). At baseline, posttreatment, and 1 year, depressive symptoms were assessed, and whole body insulin sensitivity (WBISI) was estimated from oral glucose tolerance tests. Dual energy X-ray absorptiometry assessed fat mass at baseline and 1 year. Primary outcomes were 1-year changes in depression and insulin sensitivity, adjusting for adiposity and other relevant covariates. Secondary outcomes were fasting and 2-hr insulin and glucose. We also evaluated the moderating effect of baseline depressive symptom severity. RESULTS: Depressive symptoms decreased in both groups (P < .001). Insulin sensitivity was stable in CBT and HE (ΔWBISI: .1 vs. .3) and did not differ between groups (P = .63). However, among girls with greater (moderate) baseline depressive symptoms (N = 78), those in CBT developed lower 2-hr insulin than those in HE (Δ-16 vs. 16 µIU/mL, P < .05). Additional metabolic benefits of CBT were seen for this subgroup in post hoc analyses of posttreatment to 1-year change. CONCLUSIONS: Adolescent females at risk for T2D decreased depressive symptoms and stabilized insulin sensitivity 1 year following brief CBT or HE. Further studies are required to determine if adolescents with moderate depression show metabolic benefits after CBT.

Associations of adolescent emotional and loss of control eating with 1-year changes in disordered eating, weight, and adiposity.

OBJECTIVE: Adolescent emotional-eating, referring to eating in response to negative affective states, is frequently reported by those with loss of control (LOC) eating. Although LOC eating has been shown to predict exacerbated disordered eating and excess weight/adiposity gain, the extent to which emotional-eating, either alone or in combination with LOC, predicts adverse outcomes has not been determined. Thus, we examined associations of baseline emotional-eating with changes in disordered eating, BMI, and adiposity over 1-year, and to what degree the presence or absence of baseline LOC moderated these associations. METHODS: 189 non-treatment-seeking youth (15.4 ± 1.4y; 66% female; 67% non-Hispanic White, 38% overweight [BMI ≥ 85th %ile]) completed the emotional-eating Scale for Children/Adolescents and the Eating Disorder Examination interview at baseline and again at 1-year. Air displacement plethysmography assessed adiposity at both time points. RESULTS: Baseline emotional-eating alone was not significantly associated with the development of objective binge eating or changes in disordered eating attitudes, BMI or adiposity 1-year later. However, baseline emotional-eating interacted with the presence of baseline LOC in the prediction of 1-year outcomes. Among adolescents with LOC eating, greater baseline emotional-eating was related to increased disordered eating attitudes (p = .03), BMI (p = .04), and adiposity (p = .04) at 1-year, after correcting for false discovery rate. DISCUSSION: Emotional-eating among youth also reporting LOC was associated with adverse outcomes over 1-year. Adolescents who report both behaviors may represent a subset of individuals at especially high risk for exacerbated disordered eating and excess weight gain. © 2016 Wiley Periodicals, Inc.(Int J Eat Disord 2017; 50:551-560).

A Randomized Controlled Trial to Prevent Depression and Ameliorate Insulin Resistance in Adolescent Girls at Risk for Type 2 Diabetes.

BACKGROUND: Prospective data suggest depressive symptoms worsen insulin resistance and accelerate type 2 diabetes (T2D) onset. PURPOSE: We sought to determine whether reducing depressive symptoms in overweight/obese adolescents at risk for T2D would increase insulin sensitivity and mitigate T2D risk. METHOD: We conducted a parallel-group, randomized controlled trial comparing a 6-week cognitive-behavioral (CB) depression prevention group with a 6-week health education (HE) control group in 119 overweight/obese adolescent girls with mild-to-moderate depressive symptoms (Center for Epidemiological Studies-Depression Scale [CES-D] ≥16) and T2D family history. Primary outcomes were baseline to post-intervention changes in CES-D and whole body insulin sensitivity index (WBISI), derived from 2-h oral glucose tolerance tests. Outcome changes were compared between groups using ANCOVA, adjusting for respective baseline outcome, puberty, race, facilitator, T2D family history degree, baseline age, adiposity, and adiposity change. Multiple imputation was used for missing data. RESULTS: Depressive symptoms decreased (p < 0.001) in CB and HE from baseline to posttreatment, but did not differ between groups (ΔCESD = -12 vs. -11, 95 % CI difference = -4 to +1, p = 0.31). Insulin sensitivity was stable (p > 0.29) in CB and HE (ΔWBISI = 0.1 vs. 0.2, 95 % CI difference = -0.6 to +0.4, p = 0.63). Among all participants, reductions in depressive symptoms were associated with improvements in insulin sensitivity (p = 0.02). CONCLUSIONS: Girls at risk for T2D displayed reduced depressive symptoms following 6 weeks of CB or HE. Decreases in depressive symptoms related to improvements in insulin sensitivity. Longer-term follow-up is needed to determine whether either program causes sustained decreases in depressive symptoms and improvements in insulin sensitivity. TRIAL REGISTRATION NUMBER: The trial was registered with clinicaltrials.gov (NCT01425905).

Neural activation during anticipated peer evaluation and laboratory meal intake in overweight girls with and without loss of control eating.

The interpersonal model of loss of control (LOC) eating proposes that socially distressing situations lead to anxious states that trigger excessive food consumption. Self-reports support these links, but the neurobiological underpinnings of these relationships remain unclear. We therefore examined brain regions associated with anxiety in relation to LOC eating and energy intake in the laboratory. Twenty-two overweight and obese (BMIz: 1.9±0.4) adolescent (15.8±1.6y) girls with LOC eating (LOC+, n=10) and without LOC eating (LOC-, n=12) underwent functional magnetic resonance imaging (fMRI) during a simulated peer interaction chatroom paradigm. Immediately after the fMRI scan, girls consumed lunch ad libitum from a 10,934-kcal laboratory buffet meal with the instruction to "let yourself go and eat as much as you want." Pre-specified hypotheses regarding activation of five regions of interest were tested. Analysis of fMRI data revealed a significant group by peer feedback interaction in the ventromedial prefrontal cortex (vmPFC), such that LOC+ had less activity following peer rejection (vs. acceptance), while LOC- had increased activity (p<.005). Moreover, functional coupling between vmPFC and striatum for peer rejection (vs. acceptance) interacted with LOC status: coupling was positive for LOC+, but negative in LOC- (p<.005). Activity of fusiform face area (FFA) during negative peer feedback from high-value peers also interacted with LOC status (p<.005). A positive association between FFA activation and intake during the meal was observed among only those with LOC eating. In conclusion, overweight and obese girls with LOC eating may be distinguished by a failure to engage regions of prefrontal cortex implicated in emotion regulation in response to social distress. The relationship between FFA activation and food intake supports the notion that heightened sensitivity to incoming interpersonal cues and perturbations in socio-emotional neural circuits may lead to overeating in order to cope with negative affect elicited by social discomfort in susceptible youth.

Puberty and the manifestations of loss of control eating in children and adolescents.

OBJECTIVE: We investigated the manifestations of pediatric loss of control (LOC) eating at different stages of pubertal development. METHOD: Participants were a nonclinical sample of 468 youth (8-17 years). Physical examination determined pubertal stage. LOC eating and disordered eating attitudes were assessed with the Eating Disorder Examination. In a randomized crossover design, a subset (n = 244) ate ad libitum from two test meals designed to capture normal and LOC eating. RESULTS: There were no differences in the prevalence rates or frequency of reported LOC eating episodes across pubertal stages (ps ≥ 0.50). There were, however, puberty by LOC eating interactions in disordered eating attitudes and palatable food consumption (ps ≤ .05), even after adjusting for age and body composition. LOC eating was associated with elevated global disordered eating attitudes, weight concern, and shape concern in post-pubertal youth (ps ≤ .001), but not pre-pubertal youth (ps ≥ .49). In late-puberty, youth with LOC eating consumed less energy from protein (p < .001) and more from carbohydrate (p = .003) and snack-type foods (p = .02) than those without LOC eating, whereas endorsement of LOC eating in pre- or early-to-mid-puberty was not associated with differences in eating behavior (ps ≥ 0.20). CONCLUSIONS: Findings suggest that puberty may be a critical risk period, when LOC eating behaviors in boys and girls may become accompanied by greater weight and shape concerns and more obesogenic food consumption patterns. Interventions for LOC eating during pre-puberty should be evaluated to determine if they are particularly beneficial for the prevention of exacerbated eating disorder psychopathology and adverse weight outcomes.

Brief report: genotype, phenotype, and clinical course in five patients with PAPA syndrome (pyogenic sterile arthritis, pyoderma gangrenosum, and acne).

OBJECTIVE: To describe the genotypes, phenotypes, immunophenotypes, and treatments of PAPA syndrome (pyogenic sterile arthritis, pyoderma gangrenosum, and acne), a rare autoinflammatory disease, in 5 patients. METHODS: Clinical information was gathered from medical records and through interviews with 5 patients from 4 kindreds. PSTPIP1 (CD2BP1) exon 10 and exon 11 sequencing was performed in each patient. Neutrophil granule content and cytokine levels were determined in plasma and stimulated peripheral blood mononuclear cells (PBMCs) from patients and controls. RESULTS: We identified 2 previously described PAPA syndrome-associated PSTPIP1 mutations, A230T and E250Q, and a novel change, E250K. Disease penetrance was incomplete, with variable expressivity. The cutaneous manifestations included pathergy, cystic acne, and pyoderma gangrenosum. Interleukin-1ß (IL-1ß) and circulating neutrophil granule enzyme levels were markedly elevated in patients compared to those in controls. PBMC stimulation studies demonstrated impaired production of IL-10 and enhanced production of granulocyte-macrophage colony-stimulating factor. Good resolution of pyoderma gangrenosum was achieved in 3 patients with tumor necrosis factor α (TNFα) blockade treatment. CONCLUSION: This analysis of 5 patients demonstrates that mutations in PSTPIP1 are incompletely penetrant and variably expressed in the PAPA syndrome. Neutrophil granule proteins are markedly elevated ex vivo and in the plasma, and elevated levels might be compatible with a diagnosis of PAPA syndrome. TNFα blockade appears to be effective in treating the cutaneous manifestations of PAPA syndrome.

Diabetes-Related Gastroparesis in the Acute Care Setting: A Case Report.

Diabetes-related gastroparesis is a challenging complication of diabetes that often results in flares of intractable vomiting and recurrent hospitalizations. Currently, there is no standard of care or guidelines for the management of diabetes-related gastroparesis in the acute care setting, leading to inconsistent and suboptimal care for these patients. Consequently, patients with diabetes-related gastroparesis may have prolonged inpatient lengths of stay and frequent readmissions affecting their overall health and well-being. Successful management of diabetes-related gastroparesis requires a coordinated multimodal approach to address the different components of an acute flare, including nausea and vomiting, pain, constipation, nutrition, and dysglycemia. This case report demonstrates how the development and implementation of an acute care diabetes-related gastroparesis treatment protocol demonstrates efficacy and promise for better quality of care for this population.

Effects of the COVID-19 booster vaccine on glycemia and insulin resistance in people with type 1 diabetes: A prospective pilot study.

AIMS: Inflammation can trigger hyperglycemia in people with type 1 diabetes (T1D). Vaccines purposefully intend to cause an acute immunogenic response, and booster vaccines may cause even more potent immunologic responses. However, the effects of vaccines on glycemic control and insulin requirements in the days immediately post-vaccination remains poorly understood. The aim of this study was to examine the changes in glycemic control and insulin usage immediately preceding and following a COVID-19 booster vaccine among adults with T1D. METHODS: In this prospective cohort study of adults with T1D, participants wore blinded Dexcom G6 Pro continuous glucose monitors for 10 days. After a baseline period, participants received a COVID-19 booster vaccine, and subsequent changes in glycemic indices were evaluated. RESULTS: Among the 21 enrolled participants, 38% received a Moderna and 62% Pfizer-BioNTech booster. Compared to baseline (162.9 ± 44.1 mg/dL), mean glucose was significantly increased at Day 2 (172.8 ± 47.0 mg/dL; p = 0.04) and Day 3 (173.1 ± 45.0 mg/dL; p = 0.02) post-vaccination. Insulin resistance was also increased on Day 2 (p = 0.03). There were no differences in outcome metrics between booster vaccine manufacturers. CONCLUSIONS: These results suggest that adults with type 1 diabetes may experience transient mild glycemic elevations after receiving a COVID-19 booster vaccination. Studies examining the effects of other vaccines are warranted.

Increasing Frequency of Hemoglobin A1C Measurements in Hospitalized Patients With Diabetes: A Quality Improvement Project Using Lean Six Sigma.

BACKGROUND: The American Diabetes Association (ADA) recommends measuring A1C in all inpatients with diabetes if not performed in the prior three months. Our objective was to determine the impact of utilizing Lean Six Sigma to increase the frequency of A1C measurements in hospitalized patients. METHODS: We evaluated inpatients with diabetes mellitus consecutively admitted in a community hospital between January 2016 and June 2021, excluding those who had an A1C in the electronic health record (EHR) in the previous three months. Lean Six Sigma was utilized to define the extent of the problem and devise solutions. The intervention bundle delivered between November 2017 and February 2018 included (1) provider education on the utility of A1C, (2) more rapid turnaround of A1C results, and (3) an EHR glucose-management tab and insulin order set that included A1C. Hospital encounter and patient-level data were extracted from the EHR via bulk query. Frequency of A1C measurement was compared before (January 2016-November 2017) and after the intervention (March 2018-June 2021) using χ2 analysis. RESULTS: Demographics did not differ preintervention versus postintervention (mean age [range]: 70.9 [18-104] years, sex: 52.2% male, race: 57.0% white). A1C measurements significantly increased following implementation of the intervention bundle (61.2% vs 74.5%, P < .001). This level was sustained for more than two years following the initial intervention. Patients seen by the diabetes consult service (40.4% vs 51.7%, P < 0.001) and length of stay (mean: 135 hours vs 149 hours, P < 0.001) both increased postintervention. CONCLUSIONS: We demonstrate a novel approach in improving A1C in hospitalized patients. Lean Six Sigma may represent a valuable methodology for community hospitals to improve inpatient diabetes care.

Colchicine effects on the gut microbiome in adults with metabolic syndrome.

Obesity-induced inflammation plays a substantial role in the development of insulin resistance and type 2 diabetes. The altered gut flora in obesity can also contribute to metabolic dysregulation and systemic inflammation. However, it remains unclear how dysregulation of systemic inflammation in obesity affects the gut microbiome. We hypothesized that colchicine's systemic anti-inflammatory effects in obesity would be associated with improvements in gut microbial diversity. We conducted a secondary analysis of a double-blind randomized placebo-controlled trial, in which 40 adults with obesity, high C-reactive protein (CRP) (≥2.0 mg/L), insulin resistance (homeostatic model of insulin resistance: HOMA-IR ≥2.6 mg/L), and metabolic syndrome (MetS) were randomized to three months of colchicine 0.6 mg or placebo tablets twice daily. Serum and stool samples were collected at baseline and final visit. Gut microbiota composition was characterized from stool DNA by dual-index amplification and sequencing of 16S ribosomal RNA. Pre- and post-intervention stool samples were available for 15 colchicine- and 12 placebo-treated subjects. Circulating high sensitivity CRP (hsCRP), interleukin-6, resistin, white blood count, and neutrophils were significantly decreased in the colchicine arm as compared to placebo. However, changes in stool microbiome alpha diversity, as assessed by the Chao1, Shannon, and Pielou indices, were not significant between groups. Amplicon sequence variant counts were unchanged among all examined phyla or families. Oscillibacter was the only genus to demonstrate even a nominally significant change. Among adults with obesity and MetS, colchicine significantly improved systemic inflammation. However, this anti-inflammatory effect was not associated with significant changes in the gut microbiome. Further studies are warranted to investigate this relationship.