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Metabolic Changes In Diabetes Mellitus Ppt

Type 1 Diabetes | Sweden | Pdf | Ppt| Case Reports | Symptoms | Treatment

Type 1 Diabetes | Sweden | Pdf | Ppt| Case Reports | Symptoms | Treatment

Type 1 diabetes usually develops as a result of autoimmune pancreatic beta-cell destruction in genetically susceptible individuals. Up to 90% of patients will have autoantibodies to at least one of 3 antigens: glutamic acid decarboxylase (GAD); insulin; and a tyrosine-phosphatase-like molecule, islet auto-antigen-2 (IA-2). [20] Beta-cell destruction proceeds sub-clinically for months to years as insulitis (inflammation of the beta cell). When 80% to 90% of beta cells have been destroyed, hyper glycaemia develops. Type 1 diabetes was associated with greater fatigue. Treatment for type 1 diabetes includes: Taking insulin , Carbohydrate counting, Frequent blood sugar monitoring, Eating healthy foods ,Exercising regularly and maintaining a healthy weight blood sugar levels before meals between 70 and 130 mg/dL (3.9 to 7.2 mmol/L) and after meal Levels not higher than 180 mg/dL (10 mmol/L) two hours after eating should be maintained The European Commission Directorate General for Research and Innovation (DG RTD) and the JDRF (formerly Juvenile Diabetes Research Foundation) jointly organized a workshop held in Brussels on type 1 diabetes with the ultimate goal of defining the state-of-art in the field, identifying gaps, and brainstorming about the possibilities offered by personalized medicine approaches in this area. Renowned investigators and regulators presented the latest advances and challenges concerning type 1 diabetes. Classically, the 3untranslated region (3UTR) is that region in eukaryotic protein-coding genes from the translation termination codon to the polyA signal. It is transcribed as an integral part of the mRNA encoded by the gene. However, there exists another kind of RNA, which consists of the 3UTR alone, without all other elements in mRNA such as 5UTR and Continue reading >>

Metabolic Changes In Diabetes Mellitus & Diabetic Pregnant Women

Metabolic Changes In Diabetes Mellitus & Diabetic Pregnant Women

Presentation on theme: "METABOLIC CHANGES IN DIABETES MELLITUS & DIABETIC PREGNANT WOMEN"— Presentation transcript: 1 METABOLIC CHANGES IN DIABETES MELLITUS & DIABETIC PREGNANT WOMEN BY 2 Metabolic Pregnant Edit O 2 CO 2 2 3 Metabolic Pregnant Edit 5 + 1. Carbohydrates metabolic changes, that cause hyperglycemia + 6 + b). Decrease of glycolysis pathways ac- tivity caused by decrease of + 7 - c). Increase of glycogenolysis pathways activity in the - 8 + + + Glucagon Insulin Adenylate Phospho di- cyclase esterase + + + 9 + d). Decrease of glyco- genesis pathways activity, that caused r + 10 e). Increase of gluconeogenesis pathways activity, that 11 + + + Metabolic Pregnant Edit Glycogen Glucose Hexokinase Glucose-6 + + + 12 T.C.C + f). Decrease of TCC activity, may be caused by decrease + 13 Decrease of citrate synthase enzymes activity or lact of 14 2. Lipids metabolic changes, that cause keto acidosis, hyper- 15 Increase of hormon sensitive lipase enzymes activity in 16  Hydroxy  Methyl Glutaryl CoA ( HMG CoA ) 17 + FFA (Blood) Liver VLDL Intestin Chylomicron (TG) VLDL (TG) Insulin + 18 3. Amino acids metabolic change 20 CARBOHYDRATE METABOLIC CHANGES 21 Lipid Metabolic Changes 22 + + Glucagon Insulin epinephrin etc + + 23 III. DIABETES MELLITUS AND PREGNANCY 24 * Two reasons that cause metabolic changes in pregnant woman 1 25 * Blood glucose, amino acids and insulin level fals rapidly, and on 26 2. Gestational Diabetes Mellitus 27 * Gestational DM are generally reversible after pregnancy, 28 activity of the insulin receptor by directly interacting with - 29 3. Diabetes Mellitus that Super Imposed with Pregnancy 30 * When the giant baby is born, fetal cord is cut, fetal blood 31 Devlin, T.M. : Textbook of Biochemistry with Clinical Correlati- Continue reading >>

Pathogenesis Of Gestational Dm

Pathogenesis Of Gestational Dm

Gestational diabetes (GDM) describes a heterogeneous group of hyperglycemic metabolic disorders detected in pregnancy. The majority of women with GDM are overweight or obese, and many have latent metabolic syndrome, a genetic predisposition to type 2 diabetes, a physically inactive lifestyle and unhealthy eating habits prior to pregnancy. The risk factors for GDM are similar to those of type 2 diabetes: increased waist circumference, dyslipidemia, hypertension, polycystic ovary syndrome, increasing age, family history of diabetes and ethnicity (Asian, Hispanic). Prenatal programming may also contribute to GDM whereby nutritional stress induced by both maternal undernutrition and overnutrition or maternal hyperglycemia during pregnancy persistently alter metabolism of the offspring. A minority of women develop type 1 diabetes in pregnancy, and clinicians should be alert to this possibility, but GDM may in general be regarded as pre-type 2 diabetes. Gestational diabetes is diabetes first detected in pregnancy [1] [2] . Although type 1 diabetes is more likely to develop in pregnancy, the great majority of women have pre-type 2 diabetes, and many will go on to develop permanent diabetes later in life. If type 1 diabetes is suspected during pregnancy or after delivery, autoimmunity should be confirmed by measurement of antibodies against islet cell antigens (antibodies directed against glutamic acid decarboxylase [GADA], islet antigen-2 [IA-2A]). MODY may also present in pregnancy, and genetic testing is recommended when family history suggests that this phenotype may be present. However, in general GDM can be regarded as pre-Type 2 diabetes. Pregnancy is a state of physiological insulin resistance, and thereforerepresents a physiological model of beta-cell stress [3] [4] . Continue reading >>

Diabetes Mellitus And Pregnancy

Diabetes Mellitus And Pregnancy

Practice Essentials Gestational diabetes mellitus (GDM) is defined as glucose intolerance of variable degree with onset or first recognition during pregnancy. A study by Stuebe et al found this condition to be associated with persistent metabolic dysfunction in women at 3 years after delivery, separate from other clinical risk factors. [1] Infants of mothers with preexisting diabetes mellitus experience double the risk of serious injury at birth, triple the likelihood of cesarean delivery, and quadruple the incidence of newborn intensive care unit (NICU) admission. Gestational diabetes mellitus accounts for 90% of cases of diabetes mellitus in pregnancy, while preexisting type 2 diabetes accounts for 8% of such cases. Screening for diabetes mellitus during pregnancy Gestational diabetes The following 2-step screening system for gestational diabetes is currently recommended in the United States: Alternatively, for high-risk women or in areas in which the prevalence of insulin resistance is 5% or higher (eg, the southwestern and southeastern United States), a 1-step approach can be used by proceeding directly to the 100-g, 3-hour OGTT. The US Preventive Services Task Force (USPSTF) recommends screening for gestational diabetes mellitus after 24 weeks of pregnancy. The recommendation applies to asymptomatic women with no previous diagnosis of type 1 or type 2 diabetes mellitus. [2, 3] The recommendation does not specify whether the 1-step or 2-step screening approach would be preferable. Type 1 diabetes The disease is typically diagnosed during an episode of hyperglycemia, ketosis, and dehydration It is most commonly diagnosed in childhood or adolescence; the disease is rarely diagnosed during pregnancy Patients diagnosed during pregnancy most often present with unexpected Continue reading >>

1 Metabolic Changes In Diabetes Mellitus & Diabetic Pregnant Woman Department Of Biochemistry Siti Annisa Devi Trusda.

1 Metabolic Changes In Diabetes Mellitus & Diabetic Pregnant Woman Department Of Biochemistry Siti Annisa Devi Trusda.

1 METABOLIC CHANGES IN DIABETES MELLITUS & DIABETIC PREGNANT WOMAN DEPARTMENT OF BIOCHEMISTRY Siti Annisa Devi Trusda. Published by Jemima Poole Modified over 2 years ago Presentation on theme: "1 METABOLIC CHANGES IN DIABETES MELLITUS & DIABETIC PREGNANT WOMAN DEPARTMENT OF BIOCHEMISTRY Siti Annisa Devi Trusda." Presentation transcript: 1 1 METABOLIC CHANGES IN DIABETES MELLITUS & DIABETIC PREGNANT WOMAN DEPARTMENT OF BIOCHEMISTRY Siti Annisa Devi Trusda 2 2 CO 2 + H 2 O + urea storage fuels ADP + Pi ATP O 2 Variable metab demand Variable fuel input Humans are able to use a variable fuel input to meet a variable metabolic demand 4 4 Disposition of glucose, amino acids, and fat by various tissues in the well-fed state 5 5 I. METABOLIC CHANGES IN TYPE-1 DM ( IDDM ) 6 6 1. Carbohydrates metabolic changes, that cause hyperglycemia Defect of cells of pancreas, cause absolutely lack of insulin level a). Decrease of glucose transports into the cells that caused by low activity of glucose transporter Glucose transporters Insulin Glucose Insulin receptor + 7 7 b). Decrease of glycolysis pathways activity, that caused by low activity of three kinds of glycolytic enzymes : - glucokinase / Hexokinase - Phosphofructokinase - Pyruvate kinase 8 8 Glucose Glucokinase / hexokinase Glucose-6 P Fructose-6 P Phospho fructo kinase Fructose-1,6 bi P 2 Triose-P 2-Phosphoenol pyruvate ( PEP ) Pyruvate kinase 2-Pyruvate Note : Glycolysis is oxidation of glucose to form pyruvate or lactate Insulin + + + 9 9 c). Increase of glycogenolysis pathways activity in the liver, that caused by high activity of phosphorylase enzymes in the liver 10 10 Glycogen Phosphorylase Glucose-1 P Insulin Glucose-6 P Glucose-6 P-ase Glucose - - 11 11 Glucagon Insulin Adenylate Phospho di- cyclase esterase ATP cAMP 5 Continue reading >>

Metabolic Changes Following A 1-year Diet And Exercise Intervention In Patients With Type 2 Diabetes

Metabolic Changes Following A 1-year Diet And Exercise Intervention In Patients With Type 2 Diabetes

OBJECTIVE To characterize the relationships among long-term improvements in peripheral insulin sensitivity (glucose disposal rate [GDR]), fasting glucose, and free fatty acids (FFAs) and concomitant changes in weight and adipose tissue mass and distribution induced by lifestyle intervention in obese individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS We measured GDR, fasting glucose, and FFAs during a euglycemic clamp and adipose tissue mass and distribution, organ fat, and adipocyte size by dual-energy X-ray absorptiometry, CT scan, and adipose tissue biopsy in 26 men and 32 women in the Look-AHEAD trial before and after 1 year of diet and exercise aimed at weight loss. RESULTS Weight and fasting glucose decreased significantly (P < 0.0001) and significantly more in men than in women (−12 vs. −8% and −16 vs. −7%, respectively; P < 0.05), while FFAs during hyperinsulinemia decreased and GDR increased significantly (P < 0.00001) and similarly in both sexes (−53 vs. −41% and 63 vs. 43%; P = NS). Men achieved a more favorable fat distribution by losing more from upper compared with lower and from deeper compared with superficial adipose tissue depots (P < 0.01). Decreases in weight and adipose tissue mass predicted improvements in GDR but not in fasting glucose or fasting FFAs; however, decreases in FFAs during hyperinsulinemia significantly determined GDR improvements. Hepatic fat was the only regional fat measure whose change contributed independently to changes in metabolic variables. CONCLUSIONS Patients with type 2 diabetes undergoing a 1-year lifestyle intervention had significant improvements in GDR, fasting glucose, FFAs and adipose tissue distribution. However, changes in overall weight (adipose tissue mass) and hepatic fat were the most impo Continue reading >>

Diabetes Mellitus

Diabetes Mellitus

Diabetes mellitus (DM) describes a group a metabolic diseases that are characterized by chronic hyperglycemia (elevated blood glucose levels). The two most common forms are type 1 and type 2 diabetes mellitus. Type 1 is the result of an autoimmune response that triggers the destruction of insulin-producing β cells in the pancreas and results in an absolute insulin deficiency. Type 2, which is much more common, has a strong genetic component as well as a significant association with obesity and sedentary lifestyles. Type 2 diabetes is characterized by insulin resistance (insufficient response of peripheral cells to insulin) and pancreatic β cell dysfunction (impaired insulin secretion), resulting in relative insulin deficiency. This form of diabetes usually remains clinically inapparent for many years. However, abnormal metabolism (prediabetic state or impaired glucose intolerance), which is associated with chronic hyperglycemia, causes microvascular and macrovascular changes that eventually result in cardiovascular, renal, retinal, and neurological complications. In addition, type 2 diabetic patients often present with other conditions (e.g. hypertension, dyslipidemia, obesity) that increase the risk of cardiovascular disease (e.g., myocardial infarction). Renal insufficiency is primarily responsible for the reduced life expectancy of patients with DM. Due to the chronic, progressive nature of type 1 and type 2 diabetes mellitus, a comprehensive treatment approach is necessary. The primary treatment goals for type 2 diabetes are the normalization of glucose metabolism and the management of risk factors (e.g., arterial hypertension). In theory, weight normalization, physical activity, and a balanced diet should be sufficient to prevent the manifestation of diabetes in Continue reading >>

Diabetes Mellitus (dm)

Diabetes Mellitus (dm)

Classification of Diabetes Mellitus According to WHO, DM can be categorised into the followings major types. 1- Primary DM: subclassified into - Type 1 DM: (Insulin Dependent Diabetes Mellitus, IDDM) due to autoimmune cause (b-cells of the pancreas is destroyed by immunoglobulins) - Type 2 DM: (Non-Insulin Dependent Diabetes Mellitus, NIDDM) due to - insulin resistance (esp. in obese persons) or - inadequate insulin production (in lean people) or - combination of both 2- Secondary DM: due to - Pancreatic disease - Endocrine disease (as in Cushing’s syndrome) - Drug-induced - Insulin receptors abnormalities (genetic) 3- Gestational : Glucose intolerance during pregnancy caused by metabolic & hormonal changes DM is diagnosed during pregnancy Requires insulin injection May disappear after birth BUT with increase risk of developing DM for mother & child Continue reading >>

Metabolic Changes In Diabetes.

Metabolic Changes In Diabetes.

Abstract Diabetes is not a single disease but a group of diseases characterised by hyperglycaemia. The most important regulator of glucose uptake from the blood is the hormone insulin, which is produced by islet beta cells and acts on insulin receptors to promote nutrient uptake and processing. A decrease in either insulin secretion or sensitivity can cause diabetes. Exposure to prolonged hyperglycaemia causes reversible and then irreversible changes to tissue metabolism and structure. These changes may be responsible for the potentially devastating complications of diabetes. Continue reading >>

Diabetes Mellitus (dm)

Diabetes Mellitus (dm)

Years of poorly controlled hyperglycemia lead to multiple, primarily vascular complications that affect small vessels (microvascular), large vessels (macrovascular), or both. (For additional detail, see Complications of Diabetes Mellitus.) Microvascular disease underlies 3 common and devastating manifestations of diabetes mellitus: Microvascular disease may also impair skin healing, so that even minor breaks in skin integrity can develop into deeper ulcers and easily become infected, particularly in the lower extremities. Intensive control of plasma glucose can prevent or delay many of these complications but may not reverse them once established. Macrovascular disease involves atherosclerosis of large vessels, which can lead to Immune dysfunction is another major complication and develops from the direct effects of hyperglycemia on cellular immunity. Patients with diabetes mellitus are particularly susceptible to bacterial and fungal infections. Continue reading >>

Metabolic Effects Of Diabetes Mellitus

Metabolic Effects Of Diabetes Mellitus

1. METABOLIC EFFECTS OF DIABETES MELLITUS Thamir Diab Alotaify 2. Metabolic changes in diabetes The metabolic abnormalities of diabetes mellitus result from a deficiency of insulin which profoundly affects metabolism in three tissues: liver, muscle, and adipose tissue 3. On CHO metabolism • Hyperglycemia and ketoacidosis: Elevated levels of blood glucose and ketones are the hallmarks of untreated Type 1 diabetes mellitus • Hyperglycemia is caused by increased hepatic production of glucose, combined with diminished peripheral utilization 4. On lipids  increased mobilization of fatty acids from adipose tissue,combined with accelerated hepatic fatty acid βoxidation and synthesis of Ketone bodies. * Hypertriacylglycerolemia: Not all the fatty acids flooding the liver can be disposed of through oxidation or ketone body synthesis. These excess fatty acids are converted to triacylglycerol, which is packaged and secreted in very-low-density lipoproteins (VLDL). Chylomicrons are synthesized from dietary lipids by the intestinal mucosal cells following a meal . 5. ketogenesis Cholesterol synthesis 6. insulin↓ CVS diseases ↓CHO utilization atherosclerosis shift of energy production from CHO catabolism to another source fat oxidation↑ ↑ cholsterol synthesis ↑acetyl coA comma Diabetic ketoacidosis (DKA) ↑Ketone bodies synthesis 7. Major factors contributing to hyperglycemia observed in Type 2 diabetes. Progression of blood glucose and insulin levels in patients with Type 2 diabetes. 8. Typical progression of Type 2 diabetes. Continue reading >>

What Causes Type 2 Diabetes?

What Causes Type 2 Diabetes?

Insulin resistance and high levels of insulin and lipids all precede the development of metabolic dysfunction. Which metabolic factor is to blame? Type 2 diabetes is a multifactorial metabolic disease.1 Obesity, elevated levels of lipids and insulin in the blood, and insulin resistance all accompany the elevated blood glucose that defines diabetes. (Diabetes is defined as fasting blood glucose concentrations above 7 millimolar (mM), or above 11 mM two hours after ingestion of 75 grams of glucose.) But while researchers have made much progress in understanding these components of the metabolic dysfunction, one major question remains: What serves as the primary driver of disease? Lifestyle choices characterized by inactivity have been postulated as one possible cause. Researchers have also pointed the finger at nutrition, postulating that poor food choices can contribute to metabolic disease. However, there is thus far weak support for these hypotheses. Changing to a healthy diet typically does not result in significant weight loss or the resolution of metabolic dysfunction, and it is rare to reverse obesity or diabetes through increased exercise. Furthermore, there does not appear to be a strong relationship between body-mass index (BMI) and activity level, though exercise clearly has many other health benefits. With such macroscale factors unable to explain most cases of obesity and diabetes, scientists have looked to molecular mechanisms for answers. There are at least 40 genetic mutations known to be associated with type 2 diabetes. These genes tend to be involved in the function of pancreatic β cells, which secrete insulin in response to elevated levels of the three types of cellular fuel: sugar, fat, and protein. In healthy young adults, circulating glucose concent Continue reading >>

Reference

Reference

This purpose of this talk is to overview the 2017 American Diabetes Association Standards of Medical Care in Diabetes. These Standards comprise all of the current and key clinical practice recommendations of the American Diabetes Association. [SLIDE] 2 Reference American Diabetes Association. Standards of medical care in diabetes—2014. Diabetes Care 2014;37(suppl 1):S1 A few notes on the Standards of Care: The Association funds development of the Standards of Care and all Association position statements out of its general revenues and does not use industry support for these purposes [CLICK] The slides are organized to correspond with sections within the 2017 Standards of Care. As we go through I’ll make note of where we are within the document. [CLICK] Though not every section in the document is represented, these slides do incorporate the most salient points from the Position Statement As with all Association position statements, the Standards of Care are reviewed and approved by the Association’s Board of Directors, which includes health care professionals, scientists, and lay people. [SLIDE] 3 These Standards of Care are revised annually by the ADA’s multidisciplinary Professional Practice Committee (PPC) [CLICK] For the 2017 revision, PPC members systematically searched Medline for human studies related to each subsection and published since 1 January 2016. [CLICK] Recommendations were revised based on new evidence or, in some cases, to clarify the prior recommendations or match the strength of the word to the strength of the evidence [CLICK] A table linking the changes in the recommendations to new evidence can be reviewed at professional.diabetes.org/SOC (Standards of Care) [CLICK] The Association and the Professional Practice Committee Continue reading >>

Complications Of Diabetes Mellitus

Complications Of Diabetes Mellitus

The complications of diabetes mellitus are far less common and less severe in people who have well-controlled blood sugar levels. Acute complications include hypoglycemia and hyperglycemia, diabetic coma and nonketotic hyperosmolar coma. Chronic complications occur due to a mix of microangiopathy, macrovascular disease and immune dysfunction in the form of autoimmune disease or poor immune response, most of which are difficult to manage. Microangiopathy can affect all vital organs, kidneys, heart and brain, as well as eyes, nerves, lungs and locally gums and feet. Macrovascular problems can lead to cardiovascular disease including erectile dysfunction. Female infertility may be due to endocrine dysfunction with impaired signalling on a molecular level. Other health problems compound the chronic complications of diabetes such as smoking, obesity, high blood pressure, elevated cholesterol levels, and lack of regular exercise which are accessible to management as they are modifiable. Non-modifiable risk factors of diabetic complications are type of diabetes, age of onset, and genetic factors, both protective and predisposing have been found. Overview[edit] Complications of diabetes mellitus are acute and chronic. Risk factors for them can be modifiable or not modifiable. Overall, complications are far less common and less severe in people with well-controlled blood sugar levels.[1][2][3] However, (non-modifiable) risk factors such as age at diabetes onset, type of diabetes, gender and genetics play a role. Some genes appear to provide protection against diabetic complications, as seen in a subset of long-term diabetes type 1 survivors without complications .[4][5] Statistics[edit] As of 2010, there were about 675,000 diabetes-related emergency department (ED) visits in the Continue reading >>

Type 2 Diabetes Mellitus And The Catabolic Response To Surgery | Anesthesiology | Asa Publications

Type 2 Diabetes Mellitus And The Catabolic Response To Surgery | Anesthesiology | Asa Publications

Type 2 Diabetes Mellitus and the Catabolic Response to Surgery * Assistant Professor, Biochemist, # Resident, ** Professor, Department of Anesthesia, Assistant Professor, Nutrition and Food Science Center, Associate Professor, School of Dietetics and Human Nutrition, McGill University, Montreal, Canada. Assistant Professor, Department of Anesthesia and Intensive Care Medicine, Philipps-University Marburg, Germany. Clinical Science / Endocrine and Metabolic Systems Type 2 Diabetes Mellitus and the Catabolic Response to Surgery Anesthesiology 2 2005, Vol.102, 320-326. doi: Anesthesiology 2 2005, Vol.102, 320-326. doi: Thomas Schricker, Rejeanne Gougeon, Leopold Eberhart, Linda Wykes, Louise Mazza, George Carvalho, Franco Carli; Type 2 Diabetes Mellitus and the Catabolic Response to Surgery. Anesthesiology 2005;102(2):320-326. 2018 American Society of Anesthesiologists Type 2 Diabetes Mellitus and the Catabolic Response to Surgery You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account THE endocrine response to surgical tissue trauma is characterized by the activation of the hypothalamopituitary and sympathoadrenergic system, resulting in increased circulating concentrations of cortisol, glucagon, epinephrine, and norepinephrine. 1 All these hormones inhibit insulin secretion and/or counteract the peripheral action of insulin, leading to a state of impaired tissue insulin sensitivity. 2,3 Insulin resistance is thought to be one of the principal mechanisms responsible for the catabolic responses to surgery, including stimulated amino acid oxidation, muscle proteolysis, and gluconeogenesis along with decreased glucose utilization and hyperglycemia. 4,5 The similarity between th Continue reading >>

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