Impaired Glucose Control Research Articles

Profile of Testosterone Levels on Obesity in Its Relationship with Various Other Metabolic Syndrome (MS) Components in Adult Male Subjects

Testosterone is one of the hormones that play a role in metabolic diseases such as obesity. this hormone is associated with metabolic dysfunction, and low testosterone levels are associated with energy imbalances, impaired glucose control, reduced insulin sensitivity, and dyslipidemia. This study used a descriptive research design with a cross-sectional approach. Sampling was carried out by consecutive sampling in several health facilities in the city of Makassar from March 2018 to September 2018. As many as 62 adult male subjects aged 40-65 years were examined for testosterone levels in the morning that met the inclusion criteria and then analyzed using SPSS version 22 and values

The role of proper insulin injection technique training FOR achieving of good glycaemic control

Inappropriate injection technique leads to incorrect insulin dosing, increased pain and impaired glucose control in patients with diabetes. This review examines in detail the results of two clinical studies, the Glycemic Impact of Insulin Injection Technique (GIIIT) and the UK Lipo Study (UKLS) that examined the effect of teaching patients proper injection techniques to achieve good glycemic control.
 The GIIIT study included patients with type 1 and type 2 diabetes (1870 years) who were on a regimen of multiple daily insulin injections. They were categorised into three groups: those that received structured injection technique training using 4-mm injection needles (TN), those that received injection technique training (T) and control (C). The UKLS study included 75 patients who received structured training to reduce the risk of developing lipohypertrophy.
 Initially, deviations from proper insulin injection technique were observed in a majority of patients in both the studies. In the GIIIT study, 6 months after training under TN and T conditions, HbA1c decreased by 1%, with no observable changes under the C condition. The daily insulin dose was increased by 6 IU in all conditions. Overall, the use of 4-mm short needles reduced post-injective pain in all patients. In the UKLS study, for 6 months, the variability of glycemia and frequency of unexplained hypoglycaemia decreased as the daily dose of insulin decreased by an average 6 IU; in addition, HbA1c level decreased from 8.6% to 8.2%. Six months after the training, both studies noted a decrease in or disappearance of lipohypertrophy in the patients.
 These results indicate that proper injection technique training improves glycemic control in patients with diabetes.

Glucocorticoid activation by 11β-hydroxysteroid dehydrogenase enzymes in relation to inflammation and glycaemic control in chronic kidney disease: A cross-sectional study.

SummaryObjectivePatients with chronic kidney disease (CKD) have dysregulated cortisol metabolism secondary to changes in 11β‐hydroxysteroid dehydrogenase (11β‐HSD) enzymes. The determinants of this and its clinical implications are poorly defined.MethodsWe performed a cross‐sectional study to characterize shifts in cortisol metabolism in relation to renal function, inflammation and glycaemic control. Systemic activation of cortisol by 11β‐HSD was measured as the metabolite ratio (tetrahydrocortisol [THF]+5α‐tetrahydrocortisol [5αTHF])/tetrahydrocortisone (THE) in urine.ResultsThe cohort included 342 participants with a median age of 63 years, median estimated glomerular filtration rate (eGFR) of 28 mL/min/1.73 m2 and median urine albumin‐creatinine ratio of 35.5 mg/mmol. (THF+5αTHF)/THE correlated negatively with eGFR (Spearman's ρ = −0.116, P = 0.032) and positively with C‐reactive protein (ρ = 0.208, P < 0.001). In multivariable analysis, C‐reactive protein remained a significant independent predictor of (THF+5αTHF)/THE, but eGFR did not. Elevated (THF+5αTHF)/THE was associated with HbA1c (ρ = 0.144, P = 0.008) and diabetes mellitus (odds ratio for high vs low tertile of (THF+5αTHF)/THE 2.57, 95% confidence interval 1.47‐4.47). Associations with diabetes mellitus and with HbA1c among the diabetic subgroup were independent of eGFR, C‐reactive protein, age, sex and ethnicity.ConclusionsIn summary, glucocorticoid activation by 11β‐HSD in our cohort comprising a spectrum of renal function was associated with inflammation and impaired glucose control.

Verapamil Ameliorates Hepatic Metaflammation by Inhibiting Thioredoxin-Interacting Protein/NLRP3 Pathways.

Activation of thioredoxin-interacting protein (TXNIP)/nod-like receptor protein 3 (NLRP3) inflammasome plays a critical role in pathogenesis of non-alcoholic fatty liver disease. This study investigated the protective effects of verapamil on hepatic metaflammation in a rodent model of high-fat (HF) diet-induced obesity (DIO). DIO was induced in a subset of mice provided with HF diet (45% kcal fat). After 10 weeks of HF diet, verapamil was administered by intraperitoneal injection. The experimental groups included the following: (1) normal diet group, (2) normal diet + treatment with verapamil (VER) group, (3) HF control group, (4) HF+VER (25 mg/kg/day) group. After 1 week of each treatment, blood and liver tissues were collected, and glucose control, serum triglyceride (TG) level, inflammation, and TXNIP/NLRP3 inflammasome were analyzed. Verapamil administration caused no alteration in food intake. HF diet impaired glucose control and increased body weight and serum TG levels. Hepatic inflammation was aggravated in HF-fed mice, as demonstrated by increased levels of pro-inflammatory markers interleukin-1β (IL-1β) and IL-18 in the liver. On the other hand, verapamil administration significantly improved glucose control, body weight, and serum TG levels. Verapamil treatment also reduced pro-inflammatory marker levels. These improvements were accompanied by alterations in activation of TXNIP/NLRP3 inflammasome. The observed results demonstrate that verapamil ameliorates hepatic metaflammation by inhibiting TXNIP/NLRP3 pathways.

Exercise Improves Sleep and Sleep Improves Glucose Control

Background: 77% of people with diabetes have insomnia. Sleep disturbance results in impaired glucose control in healthy individuals or worsens glucose control in people with diabetes. Short-term sleep studies (1-6 weeks) improved glucose control and insulin resistance in obese “healthy” individuals. Few studies have tested the hypothesis that improving sleep quality will improve glucose control. Exercise has been proven to help both sleep and glucose control. We wanted to test, in this abstract, the impact of improving sleep with exercise. Methods: We recommend aerobic exercise 10 minutes after each meal (HIIT) to all our patients, but not all adhere for a variety of reasons. We also advise balance and stretch.We compared 50 non-adherent type 2 patients to a matched exercise-adherent patients. We quantified feeling of well being, shortening latency of sleep onset, and sleep duration extension. We measured their glucose control with AM insulin/glucose ratio, HgA1c, and in-target glucose when CGMS was available (12 patients). All patients followed our standard diabetes treatment protocol for type 2. Results: At 12 months, adhering to exercise improved the feeling of well being in 68%, sleep hygiene in 66% of patients; Sleep increased by 28 minutes, and sleep onset latency decreased by 8 minutes. Insulin/glucose ratio was 16/133=0.12, HgA1c 7.1%, HgA1c&amp;lt;7 in 69%, and in-target glucose in 74% on CGMS (7 patients). Non-adherent had feeling of well being in 45%, sleep hygiene in 14%; with sleep increasing by 4 minutes, and sleep onset latency decreased by 2 minutes. Insulin/Glucose ratio was 38/174=0.21, HgA1c 7.9%, HgA1c&amp;lt; 7 in 50%, and in-target-glucose in 54% on CGMS (5 patients.) diabetes medications used were 3 in both groups. Percentage needing basal insulin at the end was 8% in the exercise group, 21% in the non-adherent group. Conclusion: Exercise Improved sleep and insulin resistance with improved glucose control. However, what is the contribution of each factor will need further study. Disclosure S. Sakkal: None.

Improving Sleep by Trazodone Improves Glucose Control

Background: 77% of people with diabetes have some form of insomnia. Sleep disturbance results in impaired glucose control in healthy individuals or worsens glucose control in people with diabetes. Short-term sleep studies (1-6 weeks) improved glucose control and insulin resistance in obese “healthy” individuals. We have shown before the superior benefit Trazodone has in treating neuropathy over gabapentin. We show, in this abstract, the impact of improving sleep may have on glucose control. Methods: we treated 200 type 2 patients with diabetic neuropathy with either trazodone (100), or Gabapentin(100), compared the change in neuropathy, sleep and glucose control. We quantified their neuropathy with our previously published neuropathy grading system (Sakkal’s Scale: level of vibration sensory loss by the 128 tuning fork) we quantified their sleep with shortening latency of sleep onset, and sleep duration extension. We measured their glucose control with AM insulin-to-glucose ratio, HgA1c, and in-target glucose when CGMS was available (20 patients). We excluded patients with OSA. All patients followed our standard diabetes treatment protocol for type 2. Results: At 12 months, Trazodone improved the scale of diabetic neuropathy in 80% of patients, sleep hygiene in 70%; Sleep increased by 40 minutes, and sleep onset latency decreased by 10 minutes. Insulin/glucose ratio was 21/142=0.147, HgA1c 7.2%, HgA1c&amp;lt;7 in 68%, and in-target glucose in 72% on CGMS(12 patients). Gabapentin improved the scale of diabetic neuropathy in 66%, sleep hygiene in 44%; with sleep increasing by 14 minutes, and sleep onset latency decreased by 4 minutes. Insulin -to-Glucose ratio was 33/166=0.19, HgA1c 7.8%,HgA1c,7 in 56%, and in-target-glucose in 58% on CGMS (8 patients.) analysis. A maximum number of diabetes medications used were 3 in both groups. Percentage needing basal insulin at the end was 12% in the Trazodone group, 21% in the Gabapentin group. Conclusion: Improved sleep and neuropathy with Trazodone improved glucose control. Disclosure S. Sakkal: None.

Saccharin Does Not Affect Insulin Resistance in 14 Overweight Adults without Diabetes

Background: Most non-caloric artificial sweeteners (NAS) are not digested, but come in contact with the gut microbiota, an interaction that has been associated with impaired glucose control. We aimed to further investigate whether NAS affect insulin sensitivity. Methods: The study was an open label study where participants acted as their own controls before and after exposure of 240 mg saccharin/day for three months. Participants were 55-65 years old, with a body mass index of 26-29 kg/m2 without diabetes. Insulin sensitivity was assessed by use of hyperinsulinemic-euglycemic clamps and ’M value’ was calculated by dividing the glucose infusion rate during the last 60 minutes of the clamp by body weight (mg/kg/min). Results: Of the 14 included participants, one did not complete the study. There was no change in insulin resistance after exposure to saccharin. The mean M value difference (∆M) for all participants was 0.0 (SD 1.6). ∆M was not related to age (p value 0.162) or sex (p value 0.578). Individual M values from the first and second insulin clamp are shown in the Figure and indicate some individual responses. Conclusions: In contrast to the larger epidemiologic studies, we did not observe a strong effect of NAS on insulin sensitivity. Some individuals exhibited impaired insulin sensitivity and we are currently investigating whether individualized responses are dependent on shifts in the gut microbiota. Disclosure K. Radholm: None. K. Kalin: None. M. Wennberg: None. M. Woodward: None. F. Bäckhed: Board Member; Self; Metabogen AB. Stock/Shareholder; Self; Metabogen AB. Advisory Panel; Self; Ferring Pharmaceuticals. O. Rolandsson: None.

Insulin Sensitivity and Glucose Homeostasis Can Be Influenced by Metabolic Acid Load.

Recent epidemiological findings suggest that high levels of dietary acid load can affect insulin sensitivity and glucose metabolism. Consumption of high protein diets results in the over-production of metabolic acids which has been associated with the development of chronic metabolic disturbances. Mild metabolic acidosis has been shown to impair peripheral insulin action and several epidemiological findings suggest that metabolic acid load markers are associated with insulin resistance and impaired glycemic control through an interference intracellular insulin signaling pathways and translocation. In addition, higher incidence of diabetes, insulin resistance, or impaired glucose control have been found in subjects with elevated metabolic acid load markers. Hence, lowering dietary acid load may be relevant for improving glucose homeostasis and prevention of type 2 diabetes development on a long-term basis. However, limitations related to patient acid load estimation, nutritional determinants, and metabolic status considerably flaws available findings, and the lack of solid data on the background physiopathology contributes to the questionability of results. Furthermore, evidence from interventional studies is very limited and the trials carried out report no beneficial results following alkali supplementation. Available literature suggests that poor acid load control may contribute to impaired insulin sensitivity and glucose homeostasis, but it is not sufficiently supportive to fully elucidate the issue and additional well-designed studies are clearly needed.

The burden of severe hypoglycemia in type 2 diabetes

Aims: More than 29 million people in the US have type 2 diabetes mellitus (T2DM), a chronic metabolic disorder characterized by a progressive deterioration of glucose control, which eventually requires insulin. Abnormally low levels of blood glucose, a feared side-effect of insulin treatment, may cause severe hypoglycemia (SHO), leading to emergency department (ED) admission, hospitalization, and long-term complications; these, in turn, drive up the costs of T2DM. This study’s objective was to estimate the prevalence and costs of SHO-related hospitalizations and their additional longer-term impacts on patients with T2DM using insulin.Methods: Using Truven MarketScan claims, we identified adult T2DM patients using basal and basal-bolus insulin regimens who were hospitalized for SHO (inpatient SHO patients) during 2010–2015. Two comparison groups were defined: those with outpatient SHO-related encounters only, including ED visits without hospitalization (outpatient SHO patients), and those with no SHO- or acute hyperglycemia-related events (comparison patients). Lengths of stay and SHO-related hospitalization costs were estimated, and propensity score and inverse probability weighting methods were used to adjust for baseline differences across the groups to evaluate longer-term impacts.Results: We identified 66,179 patients using basal and 81,876 patients using basal-bolus insulin, of which ∼1.1% (basal) to 3.2% (basal-bolus) experienced at least one SHO-related hospitalization. Among those who experienced SHO (i.e. those in the inpatient and outpatient SHO groups), 27% (basal) and 40% (basal-bolus) experienced at least one SHO-related hospitalization. One-third of basal and about one-quarter of basal-bolus patients were admitted directly to the hospital; the remainder were first assessed or treated in the ED. Inpatient SHO patients using basal insulin stayed in the hospital, including time in the ED, for 2.8 days and incurred $6896 in costs; patients using basal-bolus insulin stayed in the hospital for 2.6 days and incurred costs of $5802. Forty-to-fifty percent of inpatient SHO patients were hospitalized again for SHO. Inpatient SHO patients using basal insulin incurred significantly higher monthly costs after their initial SHO-related hospitalization than patients in the other two groups ($2935 vs $1819 and $1638), corresponding to 61% and 79% higher monthly costs; patients using basal-bolus insulin also incurred significantly higher monthly costs than patients in the other groups ($3606 vs $2731 and $2607), corresponding to 32% and 38% higher monthly costs.Limitations: These analyses excluded patients who did not seek ED or hospital care when faced with SHO; events may have been miscoded; and we were not able to account for clinical characteristics associated with SHO, such as insulin dose and duration of diabetes, or unmeasured confounders.Conclusions: The burden associated with SHO is not negligible. Nearly one in three patients using only basal insulin and one in four patients using basal-bolus regimens who experienced SHO were hospitalized at least once due to SHO. Not only did those patients incur the costs of their SHO hospitalization, but they also incurred at least $1,116 (62%) and $875 (70%) more per month than outpatient SHO or comparison patients. Reducing SHO events can help decrease the burden associated with SHO among patients with T2DM.

Dietary Pattern during 1991-2011 and Its Association with Cardio Metabolic Risks in Chinese Adults: The China Health and Nutrition Survey.

Increased prevalence of overweight and obesity, diabetes, hypertension, and other cardio metabolic risks has become a public health concern in China, a country undergoing nutrition transition. We investigated the dietary pattern during 1991–2011 and its association with these risks in a longitudinal study among adults; Adults in The China Health and Nutrition Survey were included. Three-day food consumption was collected by 24 h recall method. Anthropometric measures, blood pressure, fasting blood glucose and lipids was collected in 2009. Dietary pattern was generated using principal components analysis. The associations between dietary pattern and cardio metabolic risk were assessed with generalized linear regression adjusted for age, sex, and social economic status (SES). “Traditional” pattern loaded with rice, meat, and vegetables, and “Modern” pattern had high loadings of fast food, milk, and deep-fried food. “Traditional” pattern was inversely associated with cardio metabolic risks, with linear slopes ranging from −0.15 (95% confidence interval (CI): −0.18, −0.12) for hypertension to −0.67 (95% CI: −0.73, −0.60) for impaired glucose control. “Modern” pattern was associated positively with those factors, with slopes ranging 0.10 (95% CI: 0.04, 0.17) for high cholesterol to 0.42 (95% CI: 0.35, 0.49) for impaired glucose control. Dietary patterns were associated with cardio metabolic risk in Chinese adults.

Continuous Glucose Monitoring in Very Preterm Infants: A Randomized Controlled Trial.

Impaired glucose control in very preterm infants is associated with increased morbidity, mortality, and poor neurologic outcome. Strategies based on insulin titration have been unsuccessful in achieving euglycemia in absence of an increase in hypoglycemia and mortality. We sought to assess whether glucose administration guided by continuous glucose monitoring (CGM) is more effective than standard of care blood glucose monitoring in maintaining euglycemia in very preterm infants. Fifty newborns ≤32 weeks' gestation or with birth weight ≤1500 g were randomly assigned (1:1) within 48-hours from birth to receive computer-guided glucose infusion rate (GIR) with or without CGM. In the unblinded CGM group, the GIR adjustments were driven by CGM and rate of glucose change, whereas in the blinded CGM group the GIR was adjusted by using standard of care glucometer on the basis of blood glucose determinations. Primary outcome was percentage of time spent in euglycemic range (72-144 mg/dL). Secondary outcomes were percentage of time spent in mild (47-71 mg/dL) and severe (<47 mg/dL) hypoglycemia; percentage of time in mild (145-180 mg/dL) and severe (>180 mg/dL) hyperglycemia; and glucose variability. Neonates in the unblinded CGM group had a greater percentage of time spent in euglycemic range (median, 84% vs 68%, P < .001) and decreased time spent in mild (P = .04) and severe (P = .007) hypoglycemia and in severe hyperglycemia (P = .04) compared with the blinded CGM group. Use of CGM also decreased glycemic variability (SD: 21.6 ± 5.4 mg/dL vs 27 ± 7.2 mg/dL, P = .01; coefficient of variation: 22.8% ± 4.2% vs 27.9% ± 5.0%; P < .001). CGM-guided glucose titration can successfully increase the time spent in euglycemic range, reduce hypoglycemia, and minimize glycemic variability in preterm infants during the first week of life.

Survey of antiobesity drug prescribing for obese children and young people in UK primary care

ObjectivesAntiobesity drug (AOD) prescribing in children and young people (CYP) in primary care is rising with high rates of discontinuation. Little is known about prescribing in this group in terms...

The prevalence and preventability of potentially relevant drug-drug interactions in patients admitted for cardiovascular diseases: A cross-sectional study.

The aim was to describe the type and prevalence of potentially relevant drug-drug interactions (pDDIs) in a population of patients admitted for cardiovascular diseases (CVD), and management strategies for reducing the occurrence of pDDIs. A retrospective cross-sectional study was performed on Cardiology ward of University Clinical Hospital Center in Belgrade, Serbia. A total of 527 patients, with more than one prescription during hospital stay, were enrolled in this study. Data were obtained from medical records. LexiInteract was used as the screening tool. At least one potentially relevant pDDI was identified in 83.9% of patients. Occurrence was significantly more prevalent in patients with higher number of drugs, multimorbidity, longer length of stay, arrhythmia, heart failure, infectious and respiratory disease. About 13% of pDDIs exposures were accompanied with concurrent renal or liver disease, as an additional risk for DDI manifestation. Among CVD, patients with a history of myocardial infarction possessed the highest additional risk. The most common potential clinical outcome was the effect on cardiovascular system 48.5%, renal function and/or potassium 22.3%, bleeding 9.5%, impaired glucose control 6.8% and digoxin toxicity 4.6%. Main management strategies to avoid X or D class included using paracetamol instead of NSAID or alternative NSAID (38%), alternative antibiotic or antifungal (20.4%), H2 receptor antagonist instead of PPI (8.3%), avoiding therapeutic duplication (7.3%), and alternative HMG-CoA reductase inhibitor (7%). Heart rate, blood pressure, electrolytes/potassium and blood glucose could have been employed in monitoring for potential consequence of 72.2% C class pDDIs. Use of drug interaction screening tools can be beneficial risk mitigation strategy for potentially relevant pDDIs in CVD patients. DDI screening software could be linked to the patient's laboratory results or clinical data regarding renal or liver function, as an approach to reinforce DDIs alert quality.

Maternal methyl donor and cofactor supplementation in late pregnancy increases β-cell numbers at 16 days of life in growth-restricted twin lambs.

Restricted growth before birth (IUGR) increases adult risk of Type 2 diabetes by impairing insulin sensitivity and secretion. Altered fetal one-carbon metabolism is implicated in developmental programming of adult health and disease by IUGR. Therefore, we evaluated effects of maternal dietary supplementation with methyl donors and cofactors (MMDS), designed to increase fetal supply, on insulin action in the spontaneously IUGR twin lamb. In vivo glucose-stimulated insulin secretion and insulin sensitivity were measured at days 12-14 in singleton controls (CON, n = 7 lambs from 7 ewes), twins (IUGR, n = 8 lambs from 8 ewes), and twins from ewes that received MMDS (2 g rumen-protected methionine, 300 mg folic acid, 1.2 g sulfur, 0.7 mg cobalt) daily from 120 days after mating (~0.8 of term) until delivery (IUGR+MMDS, n = 8 lambs from 4 ewes). Body composition and pancreas morphometry were assessed in lambs at day 16 IUGR reduced size at birth and increased neonatal fractional growth rate. MMDS normalized long bone lengths but not other body dimensions of IUGR lambs at birth. IUGR did not impair glucose control or insulin action at days 12-14, compared with controls. MMDS increased metabolic clearance rate of insulin and increased β-cell numerical density and tended to improve insulin sensitivity, compared with untreated IUGR lambs. This demonstrates that effects of late-pregnancy methyl donor supplementation persist until at least the third week of life. Whether these effects of MMDS persist beyond early postnatal life and improve metabolic outcomes after IUGR in adults and the underlying mechanisms remain to be determined.

Basal hypersecretion of glucagon and insulin from palmitate-exposed human islets depends on FFAR1 but not decreased somatostatin secretion

In obesity fasting levels of both glucagon and insulin are elevated. In these subjects fasting levels of the free fatty acid palmitate are raised. We have demonstrated that palmitate enhances glucose-stimulated insulin secretion from isolated human islets via free fatty acid receptor 1 (FFAR1/GPR40). Since FFAR1 is also present on glucagon-secreting alpha-cells, we hypothesized that palmitate simultaneously stimulates secretion of glucagon and insulin at fasting glucose concentrations. In addition, we hypothesized that concomitant hypersecretion of glucagon and insulin was also contributed by reduced somatostatin secretion. We found basal glucagon, insulin and somatostatin secretion and respiration from human islets, to be enhanced during palmitate treatment at normoglycemia. Secretion of all hormones and mitochondrial respiration were lowered when FFAR1 or fatty acid β-oxidation was inhibited. The findings were confirmed in the human beta-cell line EndoC-βH1. We conclude that fatty acids enhance both glucagon and insulin secretion at fasting glucose concentrations and that FFAR1 and enhanced mitochondrial metabolism but not lowered somatostatin secretion are crucial in this effect. The ability of chronically elevated palmitate levels to simultaneously increase basal secretion of glucagon and insulin positions elevated levels of fatty acids as potential triggering factors for the development of obesity and impaired glucose control.

Cancer patients with undiagnosed and poorly managed diabetes mellitus.

e18232 Background: Cancer patients are at increased risk of developing diabetes mellitus (DM) or having worsening control of their pre-existent DM. The causes of this are multifactorial but the use of steroids, either in the palliative setting or short-term whilst on chemotherapy, is a significant contributor. An audit carried out at a district general hospital demonstrated that 5% of all oncology admissions were secondary to DM complications. A study was conducted to evaluate the prevalence of impaired blood glucose (BG) control and to assess the value of routine HbA1c testing in this population. Methods: Patients having routine chemotherapy blood tests were also tested for HbA1c over a 10 day period in December 2016. HbA1c diagnostic criteria was used as per NICE guidelines. Information on previous diabetic status, primary tumour type, chemotherapy status (number of cycles and treatment intent) was recorded. Results: 134 patients were tested for HbA1c; 28 (21%) had a HbA1c diagnostic of DM and 32 (24%) were at high risk of DM. The mean HbA1c of those in the DM group was 67.3 mmol/mol (range 48-120). Of the 28 with a HbA1C diagnostic of DM, 13 (46%) were already known to have DM with 15 (54%) being newly diagnosed from this study. 11 (73%) of those with a new diagnosis of DM were receiving a short course of steroids with chemotherapy. 12 patients in the DM group were having chemotherapy with curative intent; 6 of whom were newly diagnosed. Conclusions: 11% of the study cohort met criteria for a new diagnosis of DM with 73% of this group receiving steroids. NICE advises on monitoring of BG for all diabetics receiving steroids. Monitoring of BG and using anti-diabetic medications could prevent DM related complications. This highlights the need to involve local diabetic services and primary care providers for diabetic management. 43% of patients in DM group were receiving chemotherapy with curative intent. This has large implications on cancer survivorship and it is vital that these patients receive appropriate DM treatment. This will not only improve quality of care and patient satisfaction but also lead to significant cost savings from reduced admissions and length of stay in hospital. We therefore recommend a routine HbA1c test for all cancer patients having chemotherapy.

Food security is related to adult type 2 diabetes control over time in a United States safety net primary care clinic population

Background/Objectives:Successful Type 2 diabetes management requires adopting a high nutrient-density diet made up of food items that both meet dietary needs and preferences and can be feasibly obtained on a regular basis. However, access to affordable, nutrient-dense foods often is lacking in poorer neighbourhoods. Therefore, low food security should directly impair glucose control, even when patients have full access to and utilize comprehensive medical management. The present study sought to determine whether food security is related longitudinally to glucose control, over-and-above ongoing medication management, among Type 2 diabetes patients receiving comprehensive care at a Midwestern multi-site federally qualified health centre (FQHC).Subjects/Methods:In this longitudinal observational study, we completed a baseline assessment of patients’ food security (using the US Household Food Security Module), demographics (via Census items), and diabetes history/management (using a structured clinical encounter form) when patients began receiving diabetes care at the health centre. We then recorded those patients’ A1C levels several times during a 24-month follow-up period. Three hundred and ninety-nine patients (56% with low food security) had a baseline A1c measurement; a subsample of 336 (median age=52 years; 56% female; 60% Hispanic, 27% African American, and 9% White) also had at least one follow-up A1c measurement.Results:Patients with lower (vs higher) food security were more likely to be on insulin and have higher A1c levels at baseline. Moreover, the disparity in glucose control by food security status persisted throughout the next 2 years.Conclusions:Although results were based on one multi-site FQHC, potentially limiting their generalizability, they seem to suggest that among Type 2 diabetes patients, low food security directly impairs glucose control—even when patients receive full access to comprehensive medical management—thereby increasing their long-term risks of high morbidity, early mortality, and high health-care utilization and cost.

Humanin skeletal muscle protein levels increase after resistance training in men with impaired glucose metabolism

Humanin (HN) is a mitochondrially encoded and secreted peptide linked to glucose metabolism and tissue protecting mechanisms. Plasma HN levels are lower in people with type 2 diabetes. Whether skeletal muscle HN expression is influenced by exercise is unknown. Therefore, the aim of this study was to investigate serum and skeletal muscle HN levels in men with impaired glucose control in response to 12 weeks of either resistance or aerobic (nordic walking) training.Men (n=55) with impaired glucose regulation (IGR) were recruited and randomly assigned to resistance training (RT), Nordic walking (NW) or control (CON). Subjects trained three times per week for twelve weeks with progressively increased intensity during the intervention period. Biopsies from the vastus lateralis muscle and venous blood samples were taken before and after the intervention. A 2‐hr oral glucose tolerance test (OGTT) with 75 g of glucose loading was performed before and after the intervention period. Skeletal muscle and serum HN protein levels and skeletal muscle gene expression of MT‐NRN2 (the 16S gene), MT‐NRN1 (the 12S gene) and HNM1 were analyzed.Skeletal muscle HN protein levels increased by 35 % after twelve weeks of resistance training (time × group interaction p=0.022). No significant interactions over time were seen in the NW or the C groups (ns). In the RT group, ΔHN serum protein concentration was correlated to the improvement of 2‐hr glucose loading test (R= 0.597, p=0.019). Twelve weeks of either RT or NW did not change mRNA levels of MT‐NRN2, MT‐NRN1 or of HNM1. There was a significant increase in citrate synthase activity in the RT group (1.8‐fold ± 0.47 p&lt;0.05, time × group interaction p=0.027).HN protein levels in skeletal muscle increase after regular resistance training in pre‐diabetic men. The significant correlation between ΔHN serum levels and improvements in the 2‐hr time point of the OGTT suggests a role for HN in the regulation of glucose metabolism. Given the preventative effect of exercise on diabetes type 2, the role of HN as a mitochondrially derived peptide and an exercise‐responsive mitokine warrants further investigation.Support or Funding InformationThe study was supported by grants from the Research Council for Physical Education and Sports, of the Finnish Ministry of Education, of Turku University of Applied Sciences R&amp;D program and from Karolinska Institutet, Department of Physiology &amp; Pharmacology.

Ideal Cardiovascular Health, Cardiovascular Remodeling, and Heart Failure in Blacks: The Jackson Heart Study.

The lifetime risk of heart failure (HF) is higher in the black population than in other racial groups in the United States. We measured the Life's Simple 7 ideal cardiovascular health metrics in 4195 blacks in the JHS (Jackson Heart Study; 2000-2004). We evaluated the association of Simple 7 metrics with incident HF and left ventricular structure and function by cardiac magnetic resonance (n=1188). Mean age at baseline was 54.4 years (65% women). Relative to 0 to 2 Simple 7 factors, blacks with 3 factors had 47% lower incident HF risk (hazard ratio [HR], 0.53; 95% confidence interval [CI], 0.39-0.73; P<0.0001); and those with ≥4 factors had 61% lower HF risk (HR, 0.39; 95% CI, 0.24-0.64; P=0.0002). Higher blood pressure (HR, 2.32; 95% CI, 1.28-4.20; P=0.005), physical inactivity (HR, 1.65; 95% CI, 1.07-2.55; P=0.02), smoking (HR, 2.04; 95% CI, 1.43-2.91; P<0.0001), and impaired glucose control (HR, 1.76; 95% CI, 1.34-2.29; P<0.0001) were associated with incident HF. The age-/sex-adjusted population attributable risk for these Simple 7 metrics combined was 37.1%. Achievement of ideal blood pressure, ideal body mass index, ideal glucose control, and nonsmoking was associated with less likelihood of adverse cardiac remodeling by cardiac magnetic resonance. Cardiovascular risk factors in midlife (specifically elevated blood pressure, physical inactivity, smoking, and poor glucose control) are associated with incident HF in blacks and represent targets for intensified HF prevention.

Adipocyte and epidermal fatty acid-binding protein serum concentrations in patients with lipodystrophy

ObjectiveLipodystrophy (LD) syndromes are associated with diabetes mellitus, hypertriglyceridemia, and coronary artery disease. One pathogenetic factor of LD is dysregulation of several adipokines. However, the insulin resistance- and dyslipidemia-promoting adipokines adipocyte (AFABP) and epidermal (EFABP) fatty acid-binding protein have not been investigated in non-HIV-associated LD so far. Material and methodsWe performed a cross-sectional analysis of AFABP and EFABP serum concentrations in 37 LD patients and 37 age-, gender-, and body mass index-matched healthy controls. Moreover, AFABP and EFABP were correlated to clinical and biochemical parameters of inflammation, glucose control, and lipid metabolism. ResultsThere was no significant difference in median circulating AFABP and EFABP levels between LD patients (21.7μg/l and 7.5μg/l, respectively) and healthy controls (24.5μg/l and 8.6μg/l, respectively). Neither AFABP nor EFABP were related to markers of impaired glucose control or lipid metabolism. Multiple linear regression analysis showed a positive and independent association of AFABP with gender, serum leptin levels, and body mass index. ConclusionsCirculating levels of AFABP and EFABP are not decreased in LD despite adipose tissue loss in contrast to other adipokines including leptin and adiponectin.