17^th Global Diabetes Conference & Nursing Care March 8-9, 2018 | Paris, France

Biography:

Sasha Shafikhani had completed his undergraduate and PhD studies at University of California at Berkeley and Postdoctoral studies at University of California at San Francisco. He is currently an Associate Professor in the Department of Medicine at Rush University Medical Center. He serves on Editorial Board of six reputable journals. As a Cellular Microbiologist, his group conducts projects that involve bacterial pathogenesis, cancer biology and chronic wound healing

Abstract:

Persistent unresolving inflammation and enhanced bacterial infection are major co-morbidities that contribute to impaired healing in chronic diabetic foot ulcer. Given that the role of inflammatory leukocytes is to combat infection and to jumpstart healing processes, there appears to be a disconnect in the current paradigm that blames impaired healing as a culprit responsible for enhanced infection and holds enhanced infection responsible for persistent non-resolving inflammation in diabetic wound. We have used the cutaneous full-thickness wound models in STZ-injected type-1 diabetic (T1D) rats and db/db T2D mice, to study the early dynamics of inflammatory responses and bacterial infection control in normal and diabetic wound tissues. Our data indicate that in contrast to chronic diabetic foot ulcers which are locked in persistent unresolving inflammation, the acute phase of inflammatory response which is needed to counter invading pathogens early after injury and to jumpstart healing processes is significantly delayed in diabetic wound, thus rendering diabetic wound vulnerable to enhanced infection and impaired healing. Our data further suggest that normal wound tissues express pathogen-specific antimicrobial peptides that preferentially target pathogenic bacteria amongst commensals by recognizing specific virulence structure(s) that are only found in pathogenic but not commensal bacteria. In contrast, pathogen-specific antimicrobial defenses are impaired in diabetic wounds, due to inadequate inflammatory responses early after injury, thus setting the stage for the microbiome shift toward pathogenic bacteria. We further demonstrate that the inability to control pathogenic bacteria leads to persistent inflammatory state and impaired healing in diabetic wound. Importantly, we show that restoring inflammatory responses in diabetic wound early after injury enhances antimicrobial defenses and promotes healing in diabetic wound, indicating that inadequate inflammatory response early after injury in diabetic wound is just as harmful as the persistent inflammatory state that dominates these wounds as they become chronic.

Biography:

Alexander Dreval researches in areas including optimization of treatment and diagnostic methods for diabetes and its complications and mathematical modeling of endocrine systems. He has received the qualifi cation of a Mathematician at M. V. Lomonosov MSU and since 1980 he has been active in the field of mathematical modelingof insulin therapy of diabetes. He has completed PhD and Postdoctoral studies from 1st Moscow Medical Institute. He is the Director of Endocrinology Department of Moscow Regional Research Clinical Institute. He has published more than 300 papers in reputed journals and has been serving as an Editorial Board Member of repute

Abstract:

Introduction: IVGTT in diagnosing of glucose kinetics dis-balance in diabetic patients

Methodology & Theoretical Orientation: Mathematical method (one compartment model of glucose kinetics) for the analysis of Intravenous Glucose Tolerance Test (IVGTT) data is proposed that simultaneously estimates the rate of glucose disappearance from the blood (the k-value) and index of hepatic glucose production (HGP) during the test.

Findings: This method was used for IVGTT data analysis from 107 subjects: 27 diagnosed with DM2, 13 DM1 and 67 healthy volunteers. Based on application of the model to IVGTT data, two discriminant functions were obtained: Distinguishing DM2 from non-diabetic subjects and distinguishing DM1 from DM2 subjects. The 9% of non-diabetic subjects with high HGP estimates also had high k-parameter estimates. This is a pathological condition called “impaired glucose balance” (IGB) and could be considered as the earliest, pre-impaired glucose tolerance (pre-IGT) and pre-impaired fasting glucose (pre-IFG) stage of DM2. One can distinguish 4 variants of glucose dis-balance in overt diabetics depending on the k and H parameter values. It is apparent that seven subtypes of overt DM can be distinguished when one considers a combination of 4 types of glucose dis-balance and two types of DM.

Conclusion & Significance: It is theorized that various subtypes may be expected to respond in diff erent manner to different types of therapeutic interventions. In the oral presentation will be discussed diabetes diagnosing failure in IVGTT and overcome it in our modified method. This method can be useful for in choosing particular diabetic drug, that modify hepatic glucose production in diabetic patients.

Biography:

Saeko Imai is a Professor of Department of Food and Nutrition in Kyoto Women’s University, Japan. Previously, she was a Professor of Osaka Prefecture University and a Biologist with training and research experience at Molecular Nutrition at Graduated School of Life and Environmental Science in Kyoto Prefectural University. She is the Councilor of Japan Society of Metabolism and Clinical Nutrition, Japan Society of Nutrition and Food Science and Japanese Society of Nutrition and Dietetics. She is also a Member of the Japan Diabetes Society, American Diabetes Association and European Association for the Study of Diabetes. She has also authored the book “Eating order diet for Diabetes” in addition to many scientifi c and public policy articles.

Abstract:

Aim: Our aim was to explore the acute eff ect of the late-night-dinner and the divided-dinner on postprandial glucose levels in individuals with type-2 diabetes (DM) and young healthy women (NGT).

Methods: Both 16 individuals with type-2 diabetes and 14 healthy women were randomly assigned to this crossover study. Each participant wore a continuous glucose monitor for 5 days and consumed identical test meals from the second to the fourth day at home. Each participant consumed the test meals of breakfast at 08:00 h, lunch at 13:00 h and the half of the individuals consumed dinner at 21:00 h (D21) on the second day, 18:00 h (D18) on the third day and divided dinner (DD: vegetable and rice at 18:00 h and vegetable and the main dish at 21:00 h) on the fourth day. Th e rest of the individuals consumed DD on the second day and D21 on the fourth day.

Result: D21 demonstrated higher incremental glucose peak (IGP, DM: 6.78±0.79 vs. 3.09±0.62 mmol/L, p<0.01; NGT: 2.74±0.38 vs. 1.57±0.23 mmol/L, p<0.05, mean±SEM) and incremental area under the curve for glucose (IAUC) 23:00-08:00 h (DM: 644±156 vs. 147±63 mmol/L×min, p<0.01; NGT: 271±63 vs. 111±37 mmol/L×min, p<0.05) than D18. On the other hand, DD ameliorated IGP (DM: 3.75±0.58 mmol/L, p<0.01; NGT: 1.96±0.29 mmol/L, p<0.05), IAUC 23:00-08:00 h (DM: 142±60 mmol/L×min, p<0.01; NGT: 80±29 mmol/L×min, p<0.001) and the mean amplitude of glycemic excursion (DM: 5.33±0.41 vs. 6.99±0.60 mmol/L, p<0.01; NGT: 2.34±0.25 vs. 2.91±0.28 mmol/L, p<0.05) than D21 in both individuals with and without diabetes.

Conclusion: Our fi ndings demonstrated that consuming late-night-dinner led to postprandial hyperglycemia and this postprandial hyperglycemia can be ameliorated by consuming DD. Th us, DD could be a practical strategy for individuals who took late-night-dinner to reduce the postprandial glucose levels in both individuals with and without type-2 diabetes.