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COVID-19 vaccination in pregnant and lactating diabetic women.
Sculli, MA, Formoso, G, Sciacca, L
Nutrition, metabolism, and cardiovascular diseases : NMCD. 2021;(7):2151-2155
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Abstract
AIM: To discuss available information on the opportunity for pregnant women affected by diabetes/obesity to receive COVID-19 vaccine. DATA SYNTHESIS Pregnant women with SARS-CoV-2 (COVID-19) infection are at high risk for severe acute respiratory syndrome and adverse outcomes. Pregnant women with severe COVID-19 present increased rates of preterm delivery (<37 gestational weeks), cesarean delivery and neonatal admissions to the intensive care unit. Comorbidity such as diabetes (pregestational or gestational) or obesity further increased maternal and fetal complications. It is known that diabetic or obese patients with COVID-19 present an unfavorable course and a worse prognosis, with a direct association between worse outcome and suboptimal glycol-metabolic control or body mass index (BMI) levels. Critical COVID-19 infection prevention is important for both mother and fetus. Vaccination during pregnancy is a common practice. Vaccines against COVID-19 are distributed across the world with some population considered to have a priority. Since pregnant women are excluded from clinical trials very little information are available on safety and efficacy of COVD-19 vaccines during pregnancy. However, it is well known the concept of passive immunization of the newborn obtained with transplacental passage of protective antibodies into the fetal/neonatal circulation after maternal infection or vaccination. Moreover, it has been reported that COVID-19 vaccine-induced IgG pass to the neonates through breastmilk. Therefore, maternal vaccination can protect mother, fetus and baby. CONCLUSIONS After an individual risk/benefit evaluation pregnant and lactating women should be counselled to receive COVID-19 vaccines.
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Relationship between natural killer cell activity and glucose control in patients with type 2 diabetes and prediabetes.
Kim, JH, Park, K, Lee, SB, Kang, S, Park, JS, Ahn, CW, Nam, JS
Journal of diabetes investigation. 2019;(5):1223-1228
Abstract
AIMS/INTRODUCTION Natural killer (NK) cells are cytotoxic lymphocytes critical to human immunity. Previous studies showed correlations between NK cell function and blood glucose concentrations. The purpose of the present study was to assess the NK cell activity and various metabolic parameters in people with type 2 diabetes, prediabetes and normal glucose tolerance. MATERIALS AND METHODS A total of 49 participants were enrolled in the study. Anthropometric and biochemical parameters including age, sex, body mass index, smoking status, blood pressure, fasting plasma glucose, C-peptide, insulin, glycated hemoglobin, total cholesterol, triglyceride, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol were assessed. The 75 g oral glucose tolerance test was carried out for 2-h postload glucose level. Homeostatic model assessment was calculated for insulin resistance and β-cell function. NK cell activity was measured by detecting the circulating interferon-gamma level secreted from NK cells. RESULTS NK cell activity was lower in patients with type 2 diabetes (768.01 ± 650.35) compared with those with prediabetes (2,396.08 ± 653.76, P < 0.001) and normal glucose tolerance (2,435.31 ± 633.22, P < 0.001). In patients with type 2 diabetes, there was a significant inverse linear relationship between NK cell activity and fasting plasma glucose, glycated hemoglobin, and 2-h postload glucose level (all P < 0.001). Multiple regression analysis showed glycated hemoglobin to be an independent predictor of NK cell activity in patients with type 2 diabetes. CONCLUSIONS Compared with individuals with normal glucose tolerance or prediabetes, type 2 diabetes patients have a reduced NK cell activity, and it is significantly related to glucose control.
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T-lymphocyte and glycemic status after vitamin D treatment in type 1 diabetes: A randomized controlled trial with sequential crossover.
Bogdanou, D, Penna-Martinez, M, Filmann, N, Chung, TL, Moran-Auth, Y, Wehrle, J, Cappel, C, Huenecke, S, Herrmann, E, Koehl, U, et al
Diabetes/metabolism research and reviews. 2017;(3)
Abstract
BACKGROUND Type 1 diabetes mellitus (T1D) is mediated by autoaggressive T effector cells with an underlying regulatory T-cell (Treg) defect. Vitamin D deficiency is highly prevalent in T1D, which can aggravate immune dysfunction. High-dose vitamin D treatment may enhance Tregs and improve metabolism in T1D patients. METHODS In a randomized double-blind placebo-controlled trial with crossover design, patients received either for 3 months cholecalciferol 4000 IU/d followed by 3 months placebo or the sequential alternative. Thirty-nine T1D patients (19 women and 20 men) completed the trial. RESULTS Primary outcome was a change of Tregs, secondary HbA1C, and insulin demand. Effects were evaluated based on intra-individual changes between treatment and placebo periods for outcome measures. Exploratory analyses included vitamin D system variant genotyping and C-peptide measurements. Median 25(OH)D3 increased to 38.8 ng/ml with males showing a significantly stronger increase (p = .003). T-lymphocyte profiles did not change significantly (p > 2); however, the intra-individual change of Tregs between males and females was different with a significantly stronger increase in men (p = .017), as well as between genotypes of the vitamin D receptor (Apa, Taq, and Bsm: genotypes aa, TT, and bb; p = .004-0.015). Insulin demands declined significantly (p = .003-.039) and HbA1C improved (p < .001). Random C-peptide levels were low but rising (median, 0.125 ng/ml; range, 0.02-0.3) in 6 patients. No toxicity was observed. CONCLUSION A daily vitamin D dose of 4000 IU for 3 months was well tolerated and enhanced Tregs in males. Glucometabolic control improved in all. Subsequent larger trials need to address ß-cell function and genotyping for individualized vitamin D doses.
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Pathophysiology of type 1 and type 2 diabetes mellitus: a 90-year perspective.
Zaccardi, F, Webb, DR, Yates, T, Davies, MJ
Postgraduate medical journal. 2016;(1084):63-9
Abstract
Diabetes mellitus is a complex metabolic disorder associated with an increased risk of microvascular and macrovascular disease; its main clinical characteristic is hyperglycaemia. The last century has been characterised by remarkable advances in our understanding of the mechanisms leading to hyperglycaemia. The central role of insulin in glucose metabolism regulation was clearly demonstrated during the early 1920s, when Banting, Best, Collip and Macleod successfully reduced blood glucose levels and glycosuria in a patient treated with a substance purified from bovine pancreata. Later, during the mid-1930s, clinical observations suggested a possible distinction between 'insulin-sensitive' and 'insulin-insensitive' diabetes. Only during the 1950s, when a reliable measure of circulating insulin was available, was it possible to translate these clinical observations into pathophysiological and biochemical differences, and the terms 'insulin-dependent' (indicating undetectable insulin levels) and 'non-insulin-dependent' (normal or high insulin levels) started to emerge. The next 30 years were characterised by pivotal progress in the field of immunology that were instrumental in demonstrating an immune-mediated loss of insulin-secreting β-cells in subjects with 'insulin-dependent' diabetes. At the same time, new experimental techniques allowing measurement of insulin 'impedance' showed a reduced peripheral effect of insulin in subjects with 'non-insulin-dependent' diabetes (insulin resistance). The difference between the two types of diabetes emerging from decades of observations and experiments was further formally recognised in 1979, when the definitions 'type I' and 'type II' diabetes were introduced to replace the former 'insulin-dependent' and 'non-insulin-dependent' terms. In the following years, many studies elucidated the natural history and temporal contribution of insulin resistance and β-cell insulin secretion in 'type II' diabetes. Furthermore, a central role for insulin resistance in the development of a cluster of cardiometabolic alterations (dyslipidaemia, inflammation, high blood pressure) was suggested. Possibly as a consequence of the secular changes in diabetes risk factors, in the last 10 years the limitation of a simple distinction between 'type I' and 'type II' diabetes has been increasingly recognised, with subjects showing the coexistence of insulin resistance and immune activation against β-cells. With the advancement of our cellular and molecular understanding of diabetes, a more pathophysiological classification that overcomes the historical and simple 'glucocentric' view could result in a better patient phenotyping and therapeutic approach.
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The Role of Ghrelin in Senescence: A Mini-Review.
Yin, Y, Zhang, W
Gerontology. 2016;(2):155-62
Abstract
Ghrelin, a 28-amino acid hormone produced mainly by the X/A-like endocrine cells in gastric mucosa, has a widespread tissue distribution and diverse physiological functions such as hormonal, orexigenic, metabolic, cardiovascular, neurological, and immunological activities. Considerable evidence has suggested that ghrelin plays an important role in organism senescence or aging. The present review provides a comprehensive picture of this new development. We first reviewed the aging (senescence)-dependent reduction of ghrelin signaling, and then highlighted its relationship with the aging-associated alteration in food intake, energy metabolism, cardiovascular function, neurological activity, and adaptive immunity. Our literature review suggests that ghrelin is an innovative and promising agent in the treatment of these pathophysiological conditions associated with senescence.
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Metabolic Management during Critical Illness: Glycemic Control in the ICU.
Honiden, S, Inzucchi, SE
Seminars in respiratory and critical care medicine. 2015;(6):859-69
Abstract
Hyperglycemia is a commonly encountered metabolic derangement in the ICU. Important cellular pathways, such as those related to oxidant stress, immunity, and cellular homeostasis, can become deranged with prolonged and uncontrolled hyperglycemia. There is additionally a complex interplay between nutritional status, ambient glucose concentrations, and protein catabolism. While the nuances of glucose management in the ICU have been debated, results from landmark studies support the notion that for most critically ill patients moderate glycemic control is appropriate, as reflected by recent guidelines. Beyond the target population and optimal glucose range, additional factors such as hypoglycemia and glucose variability are important metrics to follow. In this regard, new technologies such as continuous glucose sensors may help alleviate the risks associated with such glucose fluctuations in the ICU. In this review, we will explore the impact of hyperglycemia upon critical cellular pathways and how nutrition provided in the ICU affects blood glucose. Additionally, important clinical trials to date will be summarized. A practical and comprehensive approach to glucose management in the ICU will be outlined, touching upon important issues such as glucose variability, target population, and hypoglycemia.
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Dipeptidyl peptidase-4 inhibitor (vildagliptin) improves glycemic control after meal tolerance test by suppressing glucagon release.
Okamoto, A, Yokokawa, H, Sanada, H
Drugs in R&D. 2014;(4):227-32
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Abstract
AIM: We aimed to evaluate changes in insulin and glucagon secretion, as well as glucose levels, with a meal tolerance test (MTT) before and after 6 months of treatment with vildagliptin in a clinical setting. MATERIALS AND METHODS Participants were 15 patients with uncontrolled type 2 diabetes mellitus (glycated hemoglobin [HbA1c] over 6.9% for more than 3 months). MTTs were conducted before and 6 months after addition of vildagliptin (50 mg twice daily [bid]). Blood samples were collected immediately before, and 1 and 2 h after the test meal for measurement of blood glucose concentration, immune-reactive insulin (IRI), and glucagon. HbA1c was measured at 6 months. RESULTS Mean age of participants was 55.5 ± 2.8 years, and ten (66.7%) were male. Mean HbA1c significantly improved from 7.6 to 6.8% at 6 months after addition of vildagliptin. Blood glucose at 1 and 2 h after the test meal was significantly reduced after addition of vildagliptin, while the reduction in glucagon showed borderline significance and IRI showed no difference. In a comparison of blood glucose-related parameters between subgroups based on median glucose change in area under the curve during MTT (ΔAUC0-2h), glucagon ΔAUC0-2h was significantly lower in the group with more improved glucose levels (ΔAUC0-2h ≥65 mg/dL), but that of IRI did not differ. CONCLUSION Suppression of glucagon release by vildagliptin may improve glycemic control without increasing insulin levels in patients with type 2 diabetes.
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Earthing the human body influences physiologic processes.
Sokal, K, Sokal, P
Journal of alternative and complementary medicine (New York, N.Y.). 2011;(4):301-8
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Abstract
OBJECTIVES This study was designed to answer the question: Does the contact of the human organism with the Earth via a copper conductor affect physiologic processes? Subjects and experiments: Five (5) experiments are presented: experiment 1-effect of earthing on calcium-phosphate homeostasis and serum concentrations of iron (N = 84 participants); experiment 2-effect of earthing on serum concentrations of electrolytes (N = 28); experiment 3-effect of earthing on thyroid function (N = 12); experiment 4-effect of earthing on glucose concentration (N = 12); experiment 5-effect of earthing on immune response to vaccine (N = 32). Subjects were divided into two groups. One (1) group of people was earthed, while the second group remained without contact with the Earth. Blood and urine samples were examined. RESULTS Earthing of an electrically insulated human organism during night rest causes lowering of serum concentrations of iron, ionized calcium, inorganic phosphorus, and reduction of renal excretion of calcium and phosphorus. Earthing during night rest decreases free tri-iodothyronine and increases free thyroxine and thyroid-stimulating hormone. The continuous earthing of the human body decreases blood glucose in patients with diabetes. Earthing decreases sodium, potassium, magnesium, iron, total protein, and albumin concentrations while the levels of transferrin, ferritin, and globulins α1, α2, β, and γ increase. These results are statistically significant. CONCLUSIONS Earthing the human body influences human physiologic processes. This influence is observed during night relaxation and during physical activity. Effect of the earthing on calcium-phosphate homeostasis is the opposite of that which occurs in states of weightlessness. It also increases the activity of catabolic processes. It may be the primary factor regulating endocrine and nervous systems.
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A randomized cross-over study of the metabolic and hormonal responses following two preoperative conditioning drinks.
Awad, S, Fearon, KC, Macdonald, IA, Lobo, DN
Nutrition (Burbank, Los Angeles County, Calif.). 2011;(9):938-42
Abstract
OBJECTIVE Preoperative conditioning with carbohydrate-based drinks attenuates postoperative insulin resistance and leads to clinical benefits. The use of metabolic conditioning agents such as glutamine and antioxidants, in addition to carbohydrate, may benefit patients undergoing major surgery, because glutamine and antioxidant supplementation have been shown to improve gastrointestinal perfusion, immune function, morbidity, and gluco-metabolic control in critically ill patients. We investigated the postprandial responses after ingestion of a clear carbohydrate drink (CCD) containing 50 g of carbohydrate (preOp, Nutricia, Trowbridge, UK) and that of another drink containing 50 g of carbohydrate, 15 g of glutamine, and antioxidants (ONS; Fresenius Kabi, Bad Homburg, Germany). METHODS Twelve overnight-fasted healthy male subjects ingested one of the drinks in a randomized, double-blinded, cross-over manner, after which blood was sampled for 360 min for measurement of glucose, insulin, glucagon, non-esterified fatty acids, β-hydroxybutyrate and glutamine. RESULTS The means ± standard errors for age and body mass index of participants were 21 ± 0.9 y and 23.2 ± 0.5 kg/m(2). After CCD ingestion, glucose and insulin concentrations peaked within 40 min (8.4 ± 0.4 mmol/L and 43.9 ± 3.8 mIU/L, respectively) and returned to baseline at 80 min (glucose 4.9 ± 0.3 mmol/L) and 140 min (insulin 5.5 ± 0.5 mIU/L). After ONS ingestion, peak glucose and insulin concentrations occurred within 40 min but were of a lower magnitude (6.6 ± 0.1 mmol/L and 29.6 ± 2.9 mIU/L, respectively). Glucose concentrations after ONS were higher than after CCD at 100 min. CONCLUSION Peak insulin and glucose concentrations were higher after CCD ingestion; in contrast, responses after ONS ingestion were "blunted" and prolonged.
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Common infections in diabetes: pathogenesis, management and relationship to glycaemic control.
Peleg, AY, Weerarathna, T, McCarthy, JS, Davis, TM
Diabetes/metabolism research and reviews. 2007;(1):3-13
Abstract
Specific defects in innate and adaptive immune function have been identified in diabetic patients in a range of in vitro studies. However, the relevance of these findings to the integrated response to infection in vivo remains unclear, especially in patients with good glycaemic control. Vaccine efficacy seems adequate in most diabetic patients, but those with type 1 diabetes and high glycosylated haemoglobin levels are most likely to exhibit hypo-responsiveness. While particular infections are closely associated with diabetes, this is usually in the context of extreme metabolic disturbances such as ketoacidosis. The link between glycaemic control and the risk of common community-acquired infections is less well established but could be clarified if infection data from large community-based observational or intervention studies were available. The relationship between hospital-acquired infections and diabetes is well recognized, particularly among post-operative cardiac and critically ill surgical patients in whom intensive insulin therapy improves clinical outcome independent of glycaemia. Nevertheless, further research is needed to improve our understanding of the role of diabetes and glycaemic control in the pathogenesis and management of community- and hospital-acquired infections.