Day 2 :
Keynote Forum
Renming Hu
Department of endocrinology of Huashan Hospital Affiliated to Fudan University Institute of Endocrinology and diabetology, at Fudan University
Keynote: Anti inflammatory treatment of diabetes and metabolic syndrome or metabolic inflammatory syndrome
Time : 09:30-10:20
Biography:
Dr Hu got the M.D and PhD from Shanghai second Medical University in 1973 and 1988. He worked the department of Endocrinology affiliated to University of Chicago during 1988-1990.
Dr Hu finished post doctor training in University of California during 1990-1993 and worked Department of Endocrinology at UCI as an assistant researcher from 1994 to 1996. He worked in Rui Jin Hospital affiliated to Shanghai Second Medical University during 1996-2002 as vice director of Institute of Endocrinogy of Shanghai and vice director of Department of Endocrinogy. He was promoted as a professor in 1999. He was director of Department of Endocrinology of Huashan Hospital affiliated to Fudan University and The Institute of Endocrinology and Diabetology at Fudan University during 2002-2010. Now Dr Hu is director of Institute of Endocrinology and Diabetology at Fudan University and director of Department of Endocrinology of Jinshan Hospital affiliated to Fudan Univesity.
Dr Hu is a council member of Chinese Diabetes association and director of the study group on microvascular complication of CDS. He is vice president of Shanghai association of diabetology. He is Editor in Chief of the Chinese edition of Diabetes Care and editorial board member Journal of Clinic Endocrinology and Metabolism and Chinese Diabetology.
Dr Hu has finished many important research projects such as Important National Nature Science Foundation of china, National High-Tech Project of china(863), National Basic Science Project of china(973), National Nature Science Foundation of china and so on. Dr Hu has published 171 papers including JCI, Diabetes, PNAS and two books in Chinese.
Abstract:
Changes in modern habits and environment produce metabolic products, including FFA and LPS, which polarize macrophages and induce chronic low grade inflammation, which damage tissues and organs and lead to metabolic diseases. Polarized macrophages not only participate in the pathophysiological process of AS, but macrophages can also invade the islets, adipocytes and liver tissues and damage these tissues and participate in the pathophysiological process of type 2 diabetes (T2DM), obesity and nonalcoholic fatty liver (NAFLD). AS, T2DM, NAFLD and obesity are closely related to chronic low grade inflammation and often accumulate, exist, or concurrency. Therefore, researchers compared AS, T2DM, NAFLD and obesity to 4 melons on a vine (chronic low inflammation), and proposed the concept and construction of metabolic inflammatory syndrome (Metabolic Inflammatory Syndrome, MIS). MIS is diagnosed as having 2 or more than 4 metabolic diseases above 4 in adition to the endocrine diseases of the known cause such as Cushing syndrome, Acromegaly and primary hypothyroidism.
The concept of MIS is in line with the theory of system biology and integrated medicine, which is beneficial to the interdisciplinary, basic and clinical combination, and to create a new method for the effective prevention and treatment of metabolic diseases with the same treatment of different diseases and the same treatment with different diseases. MIS is the development of metabolic syndrome (MS). As early as the 60-70 years of twentieth Century, researchers have found that obesity, hypertension, dyslipidemia, and diabetes are more likely to be associated with cardiovascular disease, and the combination of these metabolic risk factors is called metabolic syndrome . In 1998, WHO (WHO) expert group formally named this and put forward the diagnostic standard. Subsequently, various organizations discussed and revised their components. Microalbuminuria, impaired fasting blood glucose, or abnormality of glucose tolerance are still in the first 4 items, and the disputed risk factors include chronic low grade of inflammation (such as CRP, PAI-1), hyperuricemia, nonalcoholic fatty liver, and so on. According to the diagnostic criteria of MS, Cushing syndrome, Acromegaly and primary hypothyroidism and other diseases is also consistent with the diagnosis of MS, suggesting that MS concepts are to be discussed. The concept of MIS can better induce the metabolic diseases caused by chronic low grade inflammation. AS has become a major risk factor for human health. Therefore, screening and early diagnosis of AS is very important. The concept and diagnosis of MIS will encourage and promote T2DM, NAFLD and obese people to screen AS. Therefore, the concept of MIS is helpful for early diagnosis and prevention of AS.
Metformin and GLP-1 analogues are an effective drug for the treatment of diabetes and MIS through the indirect anti-inflammatory effects of hypoglycemic and direct anti-inflammatory effects of STAT3, which not only reduce glucose and have strong weight loss and reduce the risk of cardiovascular disease. Sulfonylureas and non sulfonylurea secretions inhibit ATP sensitive potassium channels to promote insulin secretion, and the ATP sensitive potassium channel plays a role in promoting inflammation, so this hypoglycemic agent also plays a direct and indirect way of reducing inflammation. Thiazolidone two ketones have direct and indirect mechanisms of anti-inflammatory action. Metformin, GLP-1 analogues and thiazolidinetwo can regulate STAT3, which inhibits macrophage polarization.
Dozens of anti inflammatory drugs designed for the design of interleukin, TNF and IKK beta -NF-k beta are being conducted in clinical studies, and some have been used to treat diabetes and get better results. Interleukin -1 (IL-1) receptor antagonist (Anakinra) not only significantly increases insulin secretion, but also decreases HbA1c, CRP and IL-6 in diabetic patients. And it can reduce the risk of cardiovascular events. The decrease of Foxo 1 level is closely related to dedifferentiation of beta cells, and Anakinra can significantly increase the level of Foxo1, suggesting that Anakinra may restore the function of beta cells by regulating dedifferentiation and redifferentiation.
We found that TM4(UBAC2) knockout (KO) mice developed obesity, hepatosteatosis, hypertension, and glucose intolerance under high-fat diet. TM4 counter-regulated Nur77, IKKβ, and NF-kB both in vivo and in vitro. TM4 SNP rs147851454 is significantly associated with obesity after adjusting for age and sex (OR 1.606, 95%CI 1.065-2.422 P=0.023) in 3394 non-diabetic and 1862 type 2 diabetic adults (age ≥ 19) of Han Chinese. TM4 was significantly down-regulated in the visceral fat tissue of patients with obesity who underwent laparoscopic cholecystectomy. The ubiquitin-proteasome inhibitors PS-341 and celastrol could regulate the degradation and function of TM4 and Foxo1 proteins. PS-341 and celastrol induced TM4 expression through inhibition of TM4 and Foxo1 degradation. In db/db mice, PS-341 intervention led to down-regulation of Nur77/IKKβ/NF-κB expression in visceral fat and liver, and alleviation of hyperglycemia, hypertension, and glucose intolerance. Hyperinsulinemic-euglycemic clamp demonstrated that PS-341 improved glucose infusion rate and alleviated insulin resistance in db/db mice. In conclusion, PS-341 and celastrol alleviate chronic low-grade inflammation and improves insulin sensitivity through inhibition of TM4 and Foxo1 degradation. Anti inflammatory reagents such as PS-341 and celastrol may be a candidate for the treatment of metabolic disorders including metabolic syndrome and metabolic inflammatory syndrome.
Keynote Forum
Shaodong Guo
Associate Professor, Department of Nutrition and Food Sciences, Texas A&M University, Texas 77843, U.S.A.
Keynote: Insulin Signaling, Resistance, and Metabolic Syndrome: Insights from Mouse Models into Disease Mechanisms
Time : 10:20-11:10
Biography:
Dr. Shaodong Guo is Associate Professor in the Department of Nutrition and Food Science at Texas A&M University College. He received his Ph.D in Physiology from Peking University, China. Then he completed his postdoctoral research training in Genetics, Biochemistry, and Medicine in the Chinese Academy of Sciences, the University of Illinois at Chicago, and Harvard University, respectively. Dr. Guo was an Instructor in Medicine at Children's Hospital Boston and Harvard Medical School for two years prior to joining the faculty at Texas A&M Health Science Center. Currently, Dr. Guo serves as senior editor for the Journal of Endocrinology and Journal of Molecular Endocrinology, two major official journals of Endocrine Society of Europe, UK, and Australia, and he is the textbook chapter writer for Metabolic Syndrome edited by Rexford Ahima and published by Springer in 2016. Dr. Guo lab research focuses on insulin/glucagon and estrogen signal transduction, insulin resistance, gene transcriptional control of nutrient homeostasis, and cardiac dysfunction in diabetes. Dr. Guo has been working on the gene transcriptional regulation of metabolic homeostasis by insulin receptor substrate proteins (IRS) and Forkhead FoxO transcription factors and he has been funded by American Diabetes Association (ADA), American Heart Association, and the National Institute of Health of USA. He is a recipient of ADA junior faculty award, career development award, and Richard R. Lee Award. His work has been published in a number of journals including the JBC, Endocrinology, Hypertension, Diabetes, Circulation Research, AJP, MCB, and Nature Medicine, receiving more than 5,000 citations from the Google Scholar.
Abstract:
Insulin resistance serves as the major mechanism for the development of obesity, which is pandemic in population worldwide over the past decades, largely owing to over nutrition. Excess energy stores in the adipose tissue and other organs as lipids, promoting lipotoxicity and metabolic inflammation, activating intracellular protein kinases to impair insulin signaling components, and resulting in insulin resistance. Insulin resistance is the key etiologic defect that defines “metabolic syndrome”, a group of interrelated disorders, including obesity, hyperglycemia, dyslipidemia, and hypertension. Following insulin resistance, many of patients with the metabolic syndrome eventually developed pancreatic β-cell failure, which triggers the onset of type 2 diabetes mellitus (T2DM) and its complications. Our cell- and animal-based studies demonstrate that insulin and its signaling cascades normally control cell growth, metabolism and survival through activation of mitogen-activated protein kinases (MAPKs) and phosphotidylinositide-3-kinase (PI3K), of which activation of PI-3K-associated with insulin receptor substrate-1 and -2 (IRS1, 2) and subsequent Akt→Foxo1 phosphorylation cascade has a central role in control of nutrient homeostasis and organ survival. Inactivation of Akt and activation of Foxo1, through suppression IRS1 and IRS2 in a variety of organs following over nutrition, lipotoxicity, and inflammation may form a fundamental mechanism for insulin resistance in humans. This seminar discusses the basis of insulin signaling, resistance, and how excess nutrients and lipid signaling from obesity promotes inflammation and insulin resistance, promoting organ failure with emphasis on the IRS and the forkhead/winged-helix transcription factor Foxo1.
Keynote Forum
Evangelia Litsa Tsiani
Brock University, Canada
Keynote: Antidiabetic properties of Rosemary polyphenols: Carnosol increases skeletal muscle cell glucose uptake via AMPK-dependent GLUT 4 glucose transporter translocation
Time : 11:30-12:20
Biography:
Dr Tsiani’s research focus is to investigate the biological effects and the mechanism of action of plant-derived polyphenols. She has expertise in muscle metabolism, insulin resistance, cell signaling pathways and cancer biology. Both in vitro cell culture models as well as in vivo, animal models are used in her research studies.
Normal cellular function is maintained by a complex system of signaling molecules (signaling cascades) that coordinate cell response to various stimuli. Defects in cellular signaling can lead to diseases such as diabetes (insulin resistance) and cancer. Understanding cell signaling is of major importance and provides the basis for defining novel tools for targeting signaling molecules and pathways involved in diseases. Dr Tsiani’s research has indicate strong antidiabetic and anticancer properties of plant polyphenols.
Abstract:
Statement of the Problem: Skeletal muscle is highly important in glucose homeostasis since it is quantitatively a major insulin-target tissue. Insulin action in muscle cells activates the phosphatidylinositol-3 kinase (PI3K)/Akt signaling pathway causing the translocation of intracellularly stored GLUT4 glucose transporters to the plasma membrane leading to increased glucose uptake. Impaired insulin action in muscle leads to insulin resistance and type 2 diabetes mellitus (T2DM). AMP-activated kinase (AMPK) is a cellular energy sensor and its activation increases glucose uptake by skeletal muscle cells. Finding AMPK activators is viewed as an effective approach to combat insulin resistance and T2DM. Rosemary extract (RE) has been shown to increase muscle glucose uptake and AMPK activity but the components responsible for these effects have not been identified yet. In the current study, we investigated the effect of carnosol, a polyphenol found in high concentrations in RE.
Methodology: L6 rat muscle cells were used to measure uptake of [3H]-2-deoxy-D-glucose and the signaling molecules involved were investigated by immunoblotting.
Findings: Carnosol stimulated glucose uptake in L6 myotubes in a dose- and time-dependent manner. A response comparable to maximum insulin stimulation (196+9.2 % of control) was seen with 50μM of carnosol (2h) (182+7.8 % of control). Carnosol did not affect Akt phosphorylation while it significantly increased AMPK phosphorylation. Furthermore, the increase in glucose uptake in the presence of carnosol was significantly reduced by the AMPK inhibitor compound C (CC) while it was not affected by the PI3K inhibitor wortmannin. Carnosol increased plasma membrane GLUT4 glucose transporter levels in GLUT4myc overexpressing L6 cells and this response was abolished by the AMPK inhibitor CC.
Conclusion & Significance: Our study is the first to show a significant increase in muscle glucose uptake by carnosol via a mechanism that involves AMPK. Carnosol has potential as a glucose homeostasis regulating agent and deserves further study.
- Endocrinology and Metabolic Syndrome | Obesity, Diabetes and Metabolism | Hormones and Metabolic Syndrome | Oxidative Stress and Inflammation | Endocrine and Metabolic Disorders | Metabolic Responses and Nutrition
Location: Meeting Place 3
Session Introduction
Vivek Kamath
CEO of heal the world organization
Title: Diabetes Cure for Type1, Type 2 and Type 3 (LADA)Diabetes Cure for Type1, Type 2 and Type 3 (LADA)
Time : 12:30-12:50
Biography:
Vivek Kamath founder and CEO of heal the world organization is a Reiki Master, Mexican Healer, Melchizedek Healer, Crystal Healer and Past Life Regression Therapy Expert. He has healed many diabetic patients (Type1, Type2, Type 3/1.5/LADA) without any medicines. He has also healed blood pressure (both high and low blood pressure), heart disease (removed the heart blockages), removed kidney stones, ovarian cysts, fibrosis of the breast, fatty liver, lungs disease, cured sinusitis, sever joint pain, lumbar L5 spinal disk pain, Sciatica pain, neck pain, constipation, rheumatoid arthritis, glaucoma, migraines, headaches, insomnia, stomach related problem, IBS, diabetic gum problems, skin problems( dry skin, eczema) and chronic nasal allergies, nasal blockages without any medicines. He is currently healing 5 Cancer Patients. Some are recovering from Cancer. Some of the above treatments have been completed within a week to maximum 1 month duration. Vivek Kamath received a Certificate of Recognition during 25th Global Diabetes Summit and Expo held in Dubai during December1st week in 2017 for his “Key Note Speech on Diabetes Cure”.
Abstract:
Statement of the Problem: Diabetes Type1, Type 2 and Type 3 complications.
As most of us are aware Type 2 diabetes can be controlled and cured completely with the diet, workouts (yoga), effective stress management and other healing methods. However, Type 1 and Type 1.5/3/LADA diabetes healing or complete cure is a big challenge because of our body’s immune system issue.
With type 1/1.5 diabetes, the body’s immune system attacks part of its own pancreas. Scientists are not sure why. But our immune system mistakenly sees the insulin-producing cells in the pancreas as foreign, and destroys them. This attack is considered as "autoimmune" disease. These pancreatic cells – called “islets” are the ones that sense glucose in the blood and, in response, produce the necessary amount of insulin to normalize blood sugars.
How do we protect that these “Islets” and how can we ensure that these cells produce enough insulin hormones? Using Reiki Distant Healing and telepathy techniques I have reduced 2 patients glucose level. One was type1 case of a nine-year-old boy with high fasting glucose level (350 mg/dL) and a very high random glucose level (450 to 500 mg/dL) despite of taking high dosage insulin on daily basis for nearly 2 years it was not going down. With the reiki healing techniques, it has come down to normal level within a month or so. The same experiment repeated recently on another young gentleman 38 years old patient who was suffering from Type 1.5/3/LADA disease. His FB glucose level was around 350 to 400 mg/DL from the last 8 years despite of taking strong dose of insulin on daily basis; glucose level was not going down. Within a month after initialing Reiki healing treatment, his FB glucose level came down to 190 mg/DL. He is showing recovery from diabetes. The conclusion from our healing study are that these healing and cure works mainly on 1 ) Energy level of the healer 2) Belief in self for the patients 3) Belief in Reiki Channel and universal energy 4) Intention and thought process/brain wave frequency in alpha state matching between healer and patients. If all of these things are perfect, any disease can be healed. We have made an initial breakthrough in terms of reducing their glucose level. The above study has been followed on other healing such as Lumbar L5 Spine disk pain healing. It worked amazingly and patient has shown drastic improvement in their pain relief. 80% relief on pain has been felt. We are continuing with our research on this healing for various other chronic disease cure not only type1/3 diabetes. The recent healing on Type 2 Diabetes provides us information that even if the patient has any psychological problems, it could hamper the glucose level. A Type 2 Diabetic patient’s PPBS was not going down from 290 mg/dl although his Fasting blood glucose was showing normal. We were not able to find the reason behind it. When we did the detailed consulting with the patient he was suffering from Insomnia problem. We immediately healed his insomnia problem and within few days his PPBS level came down to 110 mg/dl from 290 mg/dl. Based on these findings, it is very clear now, doctors need to find the stress factor in patient. It could be anxiety, phobia, insomnia, greed, morbid jealousy, vengeance, insecurity, depression or any chronic psychological diseases.
Fatemeh Eghbali
Ferdowsi university, Iran
Title: Effect of combined training with and without pomegranate concentrate on HbA1c and C-peptide in middle-aged women
Time : 12:50-13:15
Biography:
Ms Eghbali has graduated in sport physiology, physical activity and health from Ferdowsi university of IRAN (M.Sc in 2016). She is interested in metabolic syndrome, pre-diabetes and frailty as well as her expertise is in education patients to improve their health goals with exercise and improving lifestyle. She has years of experience in working with patients suffering from metabolic syndrome, both in hospital and education institutions.
Abstract:
Statement of the Problem: Metabolic syndrome is a cluster of metabolic disorders, such as dyslipidemia, raised blood pressure and fasting plasma glucose that can lead to diabetes type II and cardiovascular diseases. The strategy suggested for treating metabolic syndrome is to promote life style and health. Healthy lifestyle promotion and rich herb supplements with anthocyanin and polyphenol are recommended for treatment. The purpose of this research was to investigate the effects of 8 week of combined training exercise with and without pomegranate concentrate consumption on HBA1C and C-peptide in middle-aged women.
Methodology & Theoretical Orientation: In this quasi-experimental study, 24 physically inactive middle-aged¬ women suffering of metabolic syndrome participated purposively and voluntarily. The patients were randomly divided into groups of Combined exercise group (E=12) and combined exercise with pomegranate concentrate consumption group (EPC=12) who consumed pomegranate concentrate (50 gram per day for 8 weeks). The combined exercise ,aerobic and resistance, protocol were conducted with 60-80% intensity of Maximal Heart Rate (HR max), and 60-80% of One Repetition Maximal(1-RM). Participants’ HBA1c, C-peptide, anthropometry and metabolic syndrome indexes were measured once before 24-hour the first exercise session onset and a 48-hour after the last session. The data were analyzed with SPSS software. The Significance level was set at P ≤0.05.
Finding: T test results indicated a significant reduction in insulin and insulin resistance in EPC as compared to the E group. Moreover, according to the paired sample t test results, HbA1C level had a significant reduction in EPC (P≤0.05).
Conclusion & Significance: it seems that regular physical exercises along with consuming pomegranate concentrate can probably be effective through reducing HBA1c as the key index of controlling blood glucose. Through improving a number of metabolic syndrome indices such as insulin resistance it can help to prevent its resultant side effects in middle-aged women.
Lynn Ge-Zerbe
Boise Thyroid & Endocrinology PC Advanced Clinical Research, USA
Title: Genetics of metabolic disorder/obesity
Time : 14:00-14:20
Biography:
Lynn Ge-Zerbe is a recipient of the Leading Physician of the World and Pinnacle Professional of the Year 2017 award. She is board certified in Endocrinology and Internal Medicine, the Owner of Boise Thyroid & Endocrinology PC, a concierge endocrinology and weight loss practice, the Principle Investigator of Advanced Clinical Research, a Consultant Endocrinologist with RubiconMD and Video Medicine. She has earned her MD at PUMC, MPH of Epidemiology at University of Pittsburgh, Post-doctoral Fellowship in Molecular Medicine at NIH, Residency in Internal Medicine at Leigh Valley Hospital, Penn State University, Fellowship in Endocrinology at Vanderbilt University as well as Age Management Certification by AMMEF. She is passionate in combining east and west medicine to cure and prevent endocrinology disorders.
Abstract:
Worldwide 2.3 billion people are overweight caused by metabolic disorder and 1/3 of those considered obesity (WHO). More than 400 different genes have been implicated in the causes of obesity. Those genes contribute to obesity by affect appetite, satiety, metabolism, food craving, body-fat distribution and eating habit acclimate with stress etc. One of greatest example is FTO (the fat mass and obesity - associated protein) on chromosome 16q12.2 which was discovered by genome wide association study (GWAS). It's variations in intron 1 and 2 have been related to the risk of obesity and its complications. Studies suggest that FTO plays a role in controlling feeding behavior and energy expenditure.
Roux-en-Y gastric bypass (RYGB) has become a very successful treatment option for sever obesity, but not all patients lose the same amount of weight or obtain the same clinical benefits from the surgery. Studies have suggested that genetic factors explain up to 70% of the variability in weight loss after RYGB. Also, obesity was found to be associated with altered expression of a subset of genes enriched in metabolic process and mitochondrial function. After weight loss with RYGB, DNA methylation of those genes in skeletal muscle from obese patients was normalized (restored) to normal weight health controls level.
We hope that identifying the genetic factors underlying the heritable risk of obesity can contribute to our basic knowledge of the biology of energy balance, highlight molecular pathway that can be targeted for therapeutic intervention.
Omer Engin
Buca Seyfi Demirsoy State Hospital, Surgery Department, Turkey
Title: Advices to operation techniques for recurrent goitre operation
Time : 14:20-14:40
Biography:
Omer Engin is a general surgeon. He served as an scientific committee member in a lot of international conferences and as an editor a lot of international medical journals and books. His cited number is 120 and H index is 6.
Abstract:
Thyroid surgery has a lot of complications. Some of them are transient but some complications are permanent and sometime they start another complication so they are become first ring of the chain. These complications may become more than in recurrent thyroid operation. Some techniques have been developed for decreasing of these complications.
Intraoperative Nerve monitoring technique is very useful for prevent nerve injury. This technique is an EMG (electromyography) . Impulse is given to the nerve in the thyroidectomy operation area and EMG checks out in the tracheal receptor.
Another technique is methylene blue spraying method. Thyroid gland and parathyroid gland is dyed so the nerve can be seen in the operation area.
In the added to all of the technique, it should not be forgotten that carefully done operation is the most important thing. Thin tissue dissection is most important due to us. If thick tissue dissection is done in the operation, the recurrent nerve can not be seen in the thick tissue but the nerve can be seen easily in the thin dissected tissue
Cristina Bellarosa
Italian Liver Foundation
Title: Effect of Mild Hyperbilirubinemia on two in vitro models of Metabolic Syndrome
Biography:
Cristina Bellarosa, PhD is a senior scientist at Italian Liver Foundation, Trieste, Italy. She works in the field of Bilirubin since 2003 under the supervision of Prof. Claudio Tiribelli, MD. Bilirubin is one of the main research area of Italian Liver Foundation. Every two years the Foundation organize an international meeting that put together all the experts working in the field worldwide. Her scientific research activity was mainly focused on studying the molecular mechanisms of bilirubin neurotoxicity in in vitro models, with a particular focus on bilirubin cell signaling. Recently she moved to study the bilirubin protective role. She works as scientific lab tutor of PhD students, ungraduate students and fellows.
Abstract:
Background: Mildly elevated serum unconjugated bilirubin has beneficial effects on oxidative stress-mediated diseases. UGT1A1 variants in Gilbert Syndrome resulting in hyperbilirubinemia may confer a strong genetic advantage. Life-long genetically elevated bilirubin level are protective against the development of type 2 Diabetes (T2D) and the progression of nephropathy in T2D. The prevalence of hypertension was up to 25% lower in patients with bilirubin >1mg/dL, as serum levels of cholesterol and triacylglycerol. Serum bilirubin is negatively related to cardiovascular disease (CVD) and to incidence of metabolic syndrome. The protection provided by increased level of bilirubin appears to be largely due to its antioxidant and anti-inflammatory properties. Strategies to boost the bioavailability of bilirubin or to mimic Gilbert syndrome may prove to be an attractive intervention in cardiovascular disease and metabolic syndrome.
Aim: To study the protective role of mild hyperbilirubinemia on oxidative stress, inflammation and ER-stress in two in vitro models of metabolic syndrome.
Methods: Heart endothelial murine H5V cells were treated with palmitic acid (PA) and kidney tubular epithelial HK-2 cells were treated with Advanced Glycated End Products (AGE-BSA). Target genes mRNA expression, cell viability and intracellular ROS was assessed in the presence of bilirubin pretreatment or posttreatment.
Results: 24h of PA treatment on H5V cells causes cell necrosis and mRNA induction of HO-1, IL-6, GRP78 and CHOP; treatment of 72 h induces E-Selectin, V-CAM, ICAM and iNOS. UCB pre-treatment reverts cell necrosis, reduces CHOP, IL-6 and iNOS expression and increases HO-1. Treatment of HK-2 cells with AGE-BSA for 72h resulted in significative variation of IL-8, HIF1a, HO-1, GPX and Catalase mRNA expression and increases intracellular ROS. UCB pre-treatment reverses the HO1 and GPX mRNA reduction, reduces IL-8 and HIF1a mRNA induction and ROS intracellular levels. Conclusion: Bilirubin pretreatment modulates cell viability, ROS production and mRNA gene expression in the systems studied.
Gamal Moustafa
Alexandria University, Egypt
Title: Combined Treatment of HFD-induced Diabetes Mellitus by Metformin and Natural Products in Rats
Biography:
Gamal Moustafa has finished the bsc of biochemistry science, 2005. Alexandria University Egypt. Diplome of analytical biochemistry since 2012. Master degree for treatment diabetes by combination therapy till now at 2017.
Abstract:
Background: Am widely distributed over the coastal Mediterranean region. It is traditionally used in the treatment of diabetes. The aim of the present study was to evaluate the antioxidant, antihyperlipidemic and antidiabetic activity of ethyl acetate extract of AM and also study the effect of combined treatment of the extract and metformin on diabetic rats. Metformin is an oral biguanide anti hyperglycemic agent that is currently the first line therapeutic intervention in management of type 2 diabetes.
Methods: Ethyl acetate extract taken from AM tubers was used for the study. Diabetic and lipid profile, kidney and liver functions, antioxidant and anti-inflammatory parameters were performed on the experimental animals. Diabetes was induced in rat by HFD feed for 10 weeks. Rats were divided into 5 groups; control, diabetic control, treated diabetic rats I (extract 10 mg/kg+ MET 100 mg/kg), treated diabetic rats II (extract 20 mg/kg+ MET 100 mg/kg), metformin treated diabetic rats (MET 100 mg/kg). Bodyweight of each rat in the different groups was recorded daily. Biochemical and antioxidant enzyme parameters were determined on day 16.
Results: AM (combined treatment I or II?)showed better glucose utilization and insulin resistance improvement. Orally treatment of different doses of the plant extract alone and/or with metformin decreased the level of serum glucose, activity of liver alpha glucosidase, activity of pancreatic alpha amylase, MDA, CRP and leptin. Treatment showed increased level of plasma insulin, Catalase, glutathione peroxidase, liver GSH, total antioxidant capacity. Diabetic rats treated with different doses of the extract and metformin combination significantly increased muscle glucose transporter 4 (GLUT4), and remarked regenerative effect on the liver, kidney and pancreas.
Conclusion: The antioxidant, antihyperlipidemic and antidiabetic effect of ethyl acetate extract of AM and with metformin combination suggests a potential therapeutic treatment to diabetic conditions.
Keywords: Antidiabetic, Antihyperlipidemic, metformin, malondialdehyde, glucose transporter 4.
Biography:
Yasser M.Hafez has completed his PhD at the age of 35 years from school of medicine, Tanta University. He is a lecturer of internal medicine, Diabetes and Endocrinology unit. He has published this paper in reputed journal.
Abstract:
Diabetic nephropathy (DN) is one of the major causes of end-stage renal disease. Nod-like receptors nucleotide-binding domain and leucine-rich repeat pyrin-3 domain (NLRP3) inflammasome displays a considerable role in the chronic inflammatory state observed in diabetic patients. Urinary heat shock protein 72 (uHSP72) is a sensitive and specific biomarker for the early detection the acute kidney injury. The aim of this study was to evaluate NLRP3 relative gene expression, its correlation with inflammatory and oxidative stress markers, and to assess the value of uHSP72 in the early detection of DN in type 2 diabetic patients with different degrees of DN. Forty-five type 2 diabetic patients were enrolled in this study: 15 normoalbuminuric; 15 microalbuminuric; 15 macroalbuminuric patients in addition to 15 healthy controls. Clinical examination and routine laboratory investigations were done. NLRP3 mRNA expression was assessed by real time PCR. Serum 8-hydroxy-2’-deoxyguanosine (8-OHdG), IL-1β and uHSP72 levels were estimated by enzyme-linked immunosorbent assay. Serum chitotriosidase (CHIT1) activity was examined. Significant higher NLRP3 mRNA expression, serum 8-OHdG, IL-1β and uHSP72 levels, in addition to CHIT 1 activity were documented in the macroalbuminuric patient group as compared to the other two diabetic and control groups. They were significantly positively correlated and to urinary albumin/creatinine ratio, serum creatinine and HA1c. Multiple linear regression analysis using UACR as dependent variable, confirmed that uHSP72, and relative NLRP3 mRNA expression were the independent predictors of DN (β were 0.432 and 0.448 respectively, P<0.001). Receiver operating characteristic analyses revealed that both NLRP3 mRNA expression and uHSP72 levels were useful biomarkers discriminating DN patients from T2DM patients (AUC were 0.957 and 0.983 respectively) Conclusion: uHSP72 may be considered as a novel potential diagnostic biomarker for the early detection of DN. Moreover, these data support the pivotal role of NLRP3 in the development and progression of DN.
Diana Alvarado
Universidad del Valle de México, Mexico
Title: Oxidative stress and DNA damage in obese people from San Luis PotosÃ, México: accessible biomarkers to predict future disease
Biography:
Diana Alvarado has got her first Researcher Professor position in Universidad del Valle de México a year ago and became part of the Researchers National System. She has acquired experience on molecular biology and techniques to detect DNA damage, like Comet assay and Micronuclei assay, as well as the spectrophotometric techniques to detect oxidative stress. One of the reasons for which she chose as her research line obesity, is because Mexico is amongst the first world places of obesity and related diseases as obesity and metabolic syndrome. With this research line she has the purpose to show a practical, yet early way to diagnose, prevent and treat in a more specifical way, all of the comorbilities related to obesity, which have become at least in our country, the main causes for death. Passionated for her work, as a young researcher, she is looking for opportunities to establish collaboration networks with other researchers doing similar things which could be eventually translated into wellbeing for people with this disease.
Abstract:
According to the World Health Organisation, Mexico is amongst the countries with the highest prevalence of obesity and related comorbidities. Several attempts have been made in order to control this, the so called, epidemics of the century. It is imperative to design alternatives to prevent obesity-derived chronic conditions. One of the first signals of cellular impairment is oxidative stress, condition that could eventually trigger to vascular disease, immune response decreased, low repairment rate of tissues, etc. On the other hand, micronuclei has been considered as the vestibule for the development of chronical diseases, including cancer, for which we have considered of great interest to study it in association with obesity.
Statement of the Problem: Obesity has become a real problem of public health in most countries of the world, not being limited to those of high income but also to developing ones. The highest rates of obesity in adults and children are in United States of America, Mexico, New Zealand and Hungary, and it is estimated that 1 in 5 adults is obese, while 1 in 6 children are overweight or obese. Obesity is certainly the main problem, however, there is a series of comorbidities associated to obesity that make even more complicated the situation. Diseases like metabolic syndrome, diabetes, cardiovascular complications, renal failure are just some of the pathologies linked to obesity. It is of relevance the designment of strategies that allow us to deal from different perspectives with this issue. The aim of this work is, in a first phase is to detect a couple of early biomarkers (lipid ad protein peroxidation, measured as oxidative stress, and micronuclei) that could help us to associate with appearing of clinical disease during early stages; while in a second phase, to design a strategy of prevention of complications.
Methodology & Theoretical Orientation: An experimental, cross-sectional study has been designed in order to explore the levels of oxidative stress and DNA damage at different stages of the disease (obesity), trying to associate them with different factors, lifestyle, presence of other comorbidities, etc. Oxidative stress will be determined as lipid and protein peroxidation through spectrophotometric techniques, while DNA damage will be counted as micronuclei detection in oral mucose cells.
Expected findings: According to the etiology of the disease, considered as an inflammatory condition, we expected to find the highest levels in those patients with higher weight or with other pathologies, which could allow us to associate it with probable development of any other complication. It would be of usefulness to detect previously the point in which these complications could be prevented.
Conclusion & Significance: Obesity has become one of the most complicated issues in modern society. The high prevalence and incidence worldwide has made of this disease, a real public health problem. A multidisciplinary work will be definitely the path to follow, addressing this issue from different perspectives. Prevention is definitely one of the most important routes to follow, which is our main objective with this work. Mexico has one of the highest rates of obesity, and despite health sector has made enormous efforts to decrease them, it only seems to increase every year, augmenting at the same rhythm all of the complications attached to it. Designing a strategy, based on the observations at a cellular level, could allow us to prevent patients from undesirable complications, from which most of the time, they are not aware of.
We still can not conclude something clear, since our sample has not been completed yet, but we expect to end it up in the next few months.
Sarah Lim
Goulburn Valley Health, Victoria
Title: Relationship between serum zinc, glycaemic status and HOMA2 parameters in a regional Australian hospital population
Biography:
Sarah Lim is a junior doctor at Goulburn Valley Health, Victoria, Australia. She aspires to become a regional General Practitioner and has great interest in pursuing research in preventive medicine, especially Diabetes. This was her first research project, which she presented at an Annual Regional Research Fair 2017, in the presence of state-wide established researchers, stakeholders, senior clinical specialists and academics, and other non-clinical academics. An independent judge panel awarded her the Best Oral Presenter from all other established and experienced oral presenters. Sarah yearns to present this very interesting findings internationally to promote this topic and contribute to diabetes prevention globally.
Abstract:
Background: Previous studies demonstrated lower serum zinc among prediabetics and diabetics, compared to normoglycaemics. There is no current epidemiological data available in regional Australia examining the association between serum zinc and glycaemic status. This study was conducted to determine the relationship between serum zinc, glycaemic status and Homeostasis Model Assessment (HOMA-2) parameters in a regional Australian hospital population.
Methods: A retrospective review was conducted among all adult patients who presented to a regional Australian hospital between June 2004 and April 2017. Patients were included if they had either fasting blood glucose (FBG) and serum zinc; or FBG, serum zinc and fasting insulin done. Serum zinc, FBG, fasting insulin, lipid profile, vitamin D and other demographic information were collected. Beta-cell function, insulin resistance and insulin sensitivity were calculated using the HOMA-2 calculator. All data were analysed using Stata 11.
Results: A total of 313 patients’ record was retrieved. According to American Diabetic Association classification, 74.8% (234) were normoglycaemics, 18.8% (59) prediabetics and 6.4% (20) diabetics. Data for 84 patients were available to calculate HOMA-2 parameters. Mean serum zinc was found to be lower in prediabetics than normoglycaemics (14.68 ± 3.05 Vs 14.96 ± 4.01 uMol/L). In simple linear regression among all participants, higher serum zinc was associated with an increased insulin sensitivity (coefficient 2.67, 95% CI: -1.3 and 6.7), decreased insulin resistance (coefficient -0.03, 95% CI: -0.12 and 0.57) and decreased beta-cell function (coefficient -3.2, 95% CI: -6.2 and -0.2).
Conclusion: Consistent with the current literature, we observed lower serum zinc in prediabetics than normoglycaemics. Higher zinc levels are associated with greater insulin sensitivity and lower insulin resistance. Low serum zinc may have a role in the pathogenesis of insulin resistance. Further evaluations are warranted regarding zinc supplementation in prediabetics to prevent or delay the progression to Type 2 Diabetes.
- Cardiovascular Disorders | Clinical Research and Nursing Care | Herbal and Alternative Remedies | Diet and Weight Management | Advanced treatment and prevention | R&D in Endocrinology and Metabolic Disorder | Stem Cell Transplantation
Location: Meeting Place 3
Session Introduction
Eman Eladawy
Mansoura University, Egypt
Title: Relation of Anthropometric Measures and Insulin Resistance with Antimullerian Hormone in Premenopausal Women
Biography:
Eman H.EL-Adawy has completed his MD from Mansoura University. She is associate professor of Internal Medicine and Endocrinology department in Mansoura University, Spescialized Medical Hospital, Faculty of Medicine, Egypt. She has published more than 10 papers in reputed journals.
Abstract:
It has been suggested that obesity is associated with decreased level of antimullerian hormone (AMH) which considered as a good marker of ovarian reserve. Aim: The aim is to evaluate the association between obesity and AMH and whether there is relation of the anthropometric measures and insulin resistance with the level of AMH in Egyptian premenopausal women. Subjects and Methods: Eighty premenopausal women with BMI more than 30 (obese group) and 80 age-matched healthy lean women (control group). BMI, waist circumference (WC), blood pressure (BP) were measured. Fasting blood glucose (FBS), fasting insulin (FI), insulin resistance (HOMA-IR), high sensitive C-reactive protein (hs-CRP) and AMH were analyzed. Results: AMH levels in obese group were significantly lower than control group. There were significant negative correlations between each of BMI, WC, FBG, hs-CRP, FI and HOMA-IR with AMH (r = -0.214, -0.226, 0.141, -0.264, -0.241 and -0.258 respectively) (all p values ≤ 0.05). With forward stepwise linear regression analysis we found that HOMA-IR was significantly and independently related to AMH; (B = - 0.172; 95%CI -0.273: -0.071).Furthermore, HOMA-IR was confirmed to be an independent predictor of AMH after adjustment of age and BMI; (B = - 0.173; 95% CI – 0.274; - 0.072) and also by adjustment of age and WC; (B= -0.135 95%CI -0.268; -0.001). Conclusion: Obesity and insulin resistance are associated with decreased ovarian reserve among Egyptian premenopausal women.