68: Insulin Action, Insulin Resistance, And Type 2 Diabetes Mellitus
Abstract Abstract Diabetes mellitus is a syndrome characterized by elevated levels of glucose in the plasma. The American Diabetes Association has recently proposed revised criteria for the diagnosis of diabetes: (a) a fasting plasma glucose level >126 mg/dl, or (b) a plasma glucose level >200 mg/dl at 2 h after the ingestion of oral glucose (75 g), or (c) random plasma glucose >200 mg/dl. Diabetes is a heterogeneous clinical syndrome with multiple etiologies. Type 1 diabetes is caused by destruction of pancreatic beta cells, most often by autoimmune mechanisms. Type 2 diabetes (the most common form of diabetes, accounting for >90 percent of patients) is caused by a combination of two physiological defects: resistance to the action of insulin combined with a deficiency in insulin secretion. Although the molecular basis of the common form of type 2 diabetes has not been elucidated, it is thought to result from genetic defects that cause both insulin resistance and insulin deficiency. Type 2 diabetes generally has onset after the age of 40. Unlike type 1 diabetes, type 2 diabetes is usually associated with relatively mild hyperglycemia, and ketoacidosis seldom develops. Gestational diabetes mellitus is a form of diabetes that has its initial onset during pregnancy, and resolves after the end of the pregnancy. Insulin exerts multiple effects upon target cells—especially skeletal muscle, liver, and adipose tissue. In general, insulin promotes storage of fuels (e.g., glycogen and triglyceride), and inhibits the breakdown of stored fuel. To accomplish these general physiological functions, insulin exerts multiple specific actions upon target cells. For example, insulin promotes recruitment of glucose transporters from intracellular vesicles to the plasma membrane, thereby s Continue reading >>
Bromocriptine: A Dopamine Agonist For The Treatment Of Diabetes
Bromocriptine is a sympatholytic D2-dopamine agonist that has been approved for the treatment of type 2 diabetes. Based on animal and human studies, timed bromocriptine administration within 2 h of awakening is believed to augment low hypothalamic dopamine levels and inhibit excessive sympathetic tone within the central nervous system (CNS), resulting in a reduction in postmeal plasma glucose levels due to enhanced suppression of hepatic glucose production. Bromocriptine has not been shown to augment insulin secretion or enhance insulin sensitivity in peripheral tissues (muscle). Addition of bromocriptine to poorly controlled type 2 diabetic patients treated with diet alone, metformin, sulfonylureas, or thiazolidinediones produces a 0.50.7 decrement in HbA1c. Bromocriptine also reduces fasting and postmeal plasma free fatty acid (FFA) and triglyceride levels. In a 52 double-blind, placebo-controlled study in type 2 diabetic patients, bromocriptine reduced the composite cardiovascular end point by 40%. The mechanism of the drug's beneficial effect on cardiovascular disease remains to be determined. Type 2 diabetes is a chronic metabolic disorder characterized by insulin resistance, impaired -cell function, and multiple other metabolic/endocrine abnormalities.[ 1 ] Because of its multifactorial pathogenesis, restoration of normoglycemia is difficult to achieve and requires multiple antidiabetic medications that have different mechanisms of action and can be used in combination to produce an additive effect.[ 1 , 2 ] Therefore, the development of antidiabetic agents that have novel mechanisms of action and can be used in combination with currently approved medications for the treatment of type 2 diabetes is highly desirable. Type 2 diabetic patients are at high risk for a Continue reading >>
- Relative effectiveness of insulin pump treatment over multiple daily injections and structured education during flexible intensive insulin treatment for type 1 diabetes: cluster randomised trial (REPOSE)
- Is It Time to Change the Type 2 Diabetes Treatment Paradigm? No! Metformin Should Remain the Foundation Therapy for Type 2 Diabetes
- Diabetes in Dogs: Symptoms, Causes, & Treatment
The Victoza® Mechanism Of Action Works In Multiple Systems
WARNING: RISK OF THYROID C-CELL TUMORS Liraglutide causes dose-dependent and treatment-duration-dependent thyroid C-cell tumors at clinically relevant exposures in both genders of rats and mice. It is unknown whether Victoza® causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans, as the human relevance of liraglutide-induced rodent thyroid C-cell tumors has not been determined. Victoza® is contraindicated in patients with a personal or family history of MTC and in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2). Counsel patients regarding the potential risk for MTC with the use of Victoza® and inform them of symptoms of thyroid tumors (eg, a mass in the neck, dysphagia, dyspnea, persistent hoarseness). Routine monitoring of serum calcitonin or using thyroid ultrasound is of uncertain value for early detection of MTC in patients treated with Victoza®. Victoza® (liraglutide) injection 1.2 mg or 1.8 mg is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus, and to reduce the risk of major adverse cardiovascular (CV) events (CV death, non-fatal myocardial infarction, or non-fatal stroke) in adults with type 2 diabetes mellitus and established CV disease. Victoza® is not a substitute for insulin and should not be used in patients with type 1 diabetes mellitus or diabetic ketoacidosis. Concurrent use with prandial insulin has not been studied. WARNING: RISK OF THYROID C-CELL TUMORS Liraglutide causes dose-dependent and treatment-duration-dependent thyroid C-cell tumors at clinically relevant exposures in both genders of rats and mice. It is unknown whether Victoza® causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans, as the hum Continue reading >>
- Researchers identify key mechanism by which obesity causes type 2 diabetes
- Relative effectiveness of insulin pump treatment over multiple daily injections and structured education during flexible intensive insulin treatment for type 1 diabetes: cluster randomised trial (REPOSE)
- NIHR Signal Insulin pumps not much better than multiple injections for intensive control of type 1 diabetes
Mechanisms Of Current Therapies For Diabetes Mellitus Type 2
Mechanisms of current therapies for diabetes mellitus type 2 Emory University School of Medicine and Atlanta Veterans Affairs Medical Center, Decatur, Georgia Address for reprint requests and other correspondence: P. M. Thul, Emory Univ. School of Medicine and Atlanta Veterans Affairs Medical Center, Decatur, GA 30033 (e-mail: [email protected] ). Received 2012 Jun 29; Accepted 2012 Sep 21. Copyright 2012 the American Physiological Society This article has been cited by other articles in PMC. The array of medications available for the treatment of hyperglycemia has increased rapidly in the previous decade, and recent investigations have clarified novel mechanisms underlying the antihyperglycemic efficacy of these drugs. This article reviews the mechanisms of action for medications currently approved to treat diabetes mellitus in the United States, with the exception of insulin and its analogs. Finally, it attempts to integrate these mechanisms into the schema of pathophysiological factors that combine to produce hyperglycemia in patients with diabetes mellitus. Keywords: diabetes mellitus, oral agents, glucagon-like peptide-1 agonists, dipeptidyl peptidase-4 inhibitors, metformin recent investigations have clarified major aspects of type 2 diabetes mellitus (DM) pathophysiology. As demonstrated by Robert Rizza and colleagues, an oral glucose challenge increases blood sugars in subjects with mild type 2 DM more, and for a longer duration, than subjects without diabetes ( 56 ). Moreover, the expected rise in serum insulin occurs later and remains elevated longer ( 56 ). In addition to this -cell dysfunction, glucagon concentrations remain unsuppressed ( 56 ). In subjects with more pronounced diabetes, glucose levels are greater throughout the challenge, -cell dysfunction Continue reading >>
Insulin-regulatory Mechanisms And Diabetes Mellitus — Effect Of Tolbutamide On The Insulin-regulatory Mechanisms
This article has no abstract; the first 100 words appear below. STUDIES have shown that the administration of sodium tolbutamide results in a rise of the insulin content of the pancreatic venous blood of laboratory animals1 2 3 4 5 and also in the peripheral venous blood of nondiabetic human subjects and patients with non iabetes.2 , 6 These findings confirm Loubatières's7 suggestion that the sulfonylureas stimulate the pancreas and exert their action through the release of endogenous insulin. The studies reported here provide evidence that tolbutamide has at least a dual action: it stimulates the release of insulin from the pancreas and also increases the rate of utilization of the inactive form of circulating insulin both . . . *From the Protein Foundation Laboratories, Jamaica Plain, the Over-holt Thoracic Clinic, the New England Deaconess Hospital, the Joslin Clinic and the Baker Clinic Research Laboratory, Harvard Medical School. (A preliminary report appeared in Diabetes 2:34, 1962 [Supplement].) Supported by grants from the National Institutes of Health (RG-5525), National Heart Institute (HPD-16,316 and H-6302), United States Public Health Service, from the Lilly Research Laboratories and the Smith, Kleine and French Foundation. †Senior investigator, Protein Foundation Laboratories; associate staff in medicine, Peter Bent Brigham Hospital; research associate in biologic chemistry, Department of Medicine, Harvard Medical School. ‡Clinical instructor of surgery, Tufts University School of Medicine; Director, Cardiopulmonary Laboratory, and thoracic surgeon, New England Deaconess Hospital; associate, Overholt Thoracic Clinic. §Research associate in medicine, Harvard Medical School; research associate, Baker Research Laboratories; assistant in medicine, Peter Continue reading >>
- International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #59: Mechanisms of insulin signal transduction Part 3 of 8
- Effect of Probiotics on Glucose and Lipid Metabolism in Type 2 Diabetes Mellitus: A Meta-Analysis of 12 Randomized Controlled Trials
- The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus
Mechanism Of Chlorpropamide Action In Diabetes Insipidus
Mechanism of Chlorpropamide Action in Diabetes Insipidus Veterans Administration Hospital and the Department of Medicine, State University of New York, Upstate Medical Center Syracuse, New York Search for other works by this author on: Veterans Administration Hospital and the Department of Medicine, State University of New York, Upstate Medical Center Syracuse, New York Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 30, Issue 4, 1 April 1970, Pages 488496, MYRON MILLER, ARNOLD M. MOSES; Mechanism of Chlorpropamide Action in Diabetes Insipidus, The Journal of Clinical Endocrinology & Metabolism, Volume 30, Issue 4, 1 April 1970, Pages 488496, The mechanism of the antidiuretic action of chlorpropamide was studied in 13 patients with vasopressin-sensitive diabetes insipidus (DI) and in 9 normal water loaded subjects. An antidiuresis occurred in 10 of 13 patients and in all the normal subjects. A significant positive correlation was found between the ability of the patients to reduce the free water clearance (CH20) in response to water deprivation and the ability to reduce the CH20 in response to subsequent chlorpropamide treatment. Both ethanol and water loading were able to overcome the chlorpropamide-induced antidiuresis. Water deprivation while the patients were receiving chlorpropamide resulted in a further increase in urine concentration. The data indicate that, for chlorpropamide to be able to produce an antidiuresis, some low level of endogenous antidiuretic hormone (ADH) must be present. The observations can best be explained by the hypothesis that chlorpropamide is capable of potentiating the action of low, submaximal levels of endogenous ADH to result in an enhanced antidiuretic effect. No evidence of a direc Continue reading >>
Review Effects And Mechanisms Of Berberine In Diabetes Treatment
Berberine from Rhizoma Coptidis is an oral hypoglycemic agent with anti-dyslipidemia and anti-obesity activities. Its metabolic activity of regulating blood glucose and lipids has been widely studied and evidenced in patients and various animal models. Berberine is known as an AMP-activated protein kinase (AMPK) activator. Its insulin-independent hypoglycemic effect is related to inhibition of mitochondrial function, stimulation of glycolysis and activation of AMPK pathway. Additionally, berberine may also act as an α-glucosidase inhibitor. In the newly-diagnosed type 2 diabetic patients, berberine is able to lower blood insulin level via enhancing insulin sensitivity. However, in patients with poor β-cell function, berberine may improve insulin secretion via resuscitating exhausted islets. Furthermore, berberine may have extra beneficial effects on diabetic cardiovascular complications due to its cholesterol-lowering, anti-arrhythmias and nitric oxide (NO) inducing properties. The antioxidant and aldose reductase inhibitory activities of berberine may be useful in alleviating diabetic nephropathy. Although evidence from animal and human studies consistently supports the therapeutic activities of berberine, large-scale multicenter trials are still necessary to evaluate the efficacy of berberine on diabetes and its related complications. Graphical abstract The insulin-independent hypoglycemic effect of berberine is related to inhibition of mitochondrial function, stimulation of glycolysis and activation of AMPK pathway. Additionally, the antioxidant and aldose reductase inhibitory activities of berberine may be useful in alleviating diabetic nephropathy. Continue reading >>
Molecular Mechanisms Of Insulin Resistance In Type 2 Diabetes Mellitus
Molecular mechanisms of insulin resistance in type 2 diabetes mellitus Vandana Saini, Department of Biochemistry, Lady Hardinge Medical College, New Delhi 110001, India. Author contributions: Saini V contributed solely to this work. Correspondence to: Vandana Saini, MD, Department of Biochemistry, Lady Hardinge Medical College, New Delhi 110001, India. [email protected] Received 2010 Jan 18; Revised 2010 Jun 22; Accepted 2010 Jun 29. Copyright 2010 Baishideng Publishing Group Co., Limited. All rights reserved. This article has been cited by other articles in PMC. Free fatty acids are known to play a key role in promoting loss of insulin sensitivity in type 2 diabetes mellitus but the underlying mechanism is still unclear. It has been postulated that an increase in the intracellular concentration of fatty acid metabolites activates a serine kinase cascade, which leads to defects in insulin signaling downstream to the insulin receptor. In addition, the complex network of adipokines released from adipose tissue modulates the response of tissues to insulin. Among the many molecules involved in the intracellular processing of the signal provided by insulin, the insulin receptor substrate-2, the protein kinase B and the forkhead transcription factor Foxo 1a are of particular interest, as recent data has provided strong evidence that dysfunction of these proteins results in insulin resistance in vivo. Recently, studies have revealed that phosphoinositidedependent kinase 1-independent phosphorylation of protein kinase C causes a reduction in insulin receptor gene expression. Additionally, it has been suggested that mitochondrial dysfunction triggers activation of several serine kinases, and weakens insulin signal transduction. Thus, in this review, the current developmen Continue reading >>
- Resistance Training for Diabetes Prevention and Therapy: Experimental Findings and Molecular Mechanisms
- International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #59: Mechanisms of insulin signal transduction Part 3 of 8
- Is there a relationship between vitamin D with insulin resistance and diabetes mellitus?
Metformin
Metformin, marketed under the trade name Glucophage among others, is the first-line medication for the treatment of type 2 diabetes,[4][5] particularly in people who are overweight.[6] It is also used in the treatment of polycystic ovary syndrome.[4] Limited evidence suggests metformin may prevent the cardiovascular disease and cancer complications of diabetes.[7][8] It is not associated with weight gain.[8] It is taken by mouth.[4] Metformin is generally well tolerated.[9] Common side effects include diarrhea, nausea and abdominal pain.[4] It has a low risk of causing low blood sugar.[4] High blood lactic acid level is a concern if the medication is prescribed inappropriately and in overly large doses.[10] It should not be used in those with significant liver disease or kidney problems.[4] While no clear harm comes from use during pregnancy, insulin is generally preferred for gestational diabetes.[4][11] Metformin is in the biguanide class.[4] It works by decreasing glucose production by the liver and increasing the insulin sensitivity of body tissues.[4] Metformin was discovered in 1922.[12] French physician Jean Sterne began study in humans in the 1950s.[12] It was introduced as a medication in France in 1957 and the United States in 1995.[4][13] It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system.[14] Metformin is believed to be the most widely used medication for diabetes which is taken by mouth.[12] It is available as a generic medication.[4] The wholesale price in the developed world is between 0.21 and 5.55 USD per month as of 2014.[15] In the United States, it costs 5 to 25 USD per month.[4] Medical uses[edit] Metformin is primarily used for type 2 diabetes, but is increasingly be Continue reading >>
Diabetes Mellitus
"Diabetes" redirects here. For other uses, see Diabetes (disambiguation). Diabetes mellitus (DM), commonly referred to as diabetes, is a group of metabolic disorders in which there are high blood sugar levels over a prolonged period.[7] Symptoms of high blood sugar include frequent urination, increased thirst, and increased hunger.[2] If left untreated, diabetes can cause many complications.[2] Acute complications can include diabetic ketoacidosis, hyperosmolar hyperglycemic state, or death.[3] Serious long-term complications include cardiovascular disease, stroke, chronic kidney disease, foot ulcers, and damage to the eyes.[2] Diabetes is due to either the pancreas not producing enough insulin or the cells of the body not responding properly to the insulin produced.[8] There are three main types of diabetes mellitus:[2] Type 1 DM results from the pancreas's failure to produce enough insulin.[2] This form was previously referred to as "insulin-dependent diabetes mellitus" (IDDM) or "juvenile diabetes".[2] The cause is unknown.[2] Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly.[2] As the disease progresses a lack of insulin may also develop.[9] This form was previously referred to as "non insulin-dependent diabetes mellitus" (NIDDM) or "adult-onset diabetes".[2] The most common cause is excessive body weight and insufficient exercise.[2] Gestational diabetes is the third main form, and occurs when pregnant women without a previous history of diabetes develop high blood sugar levels.[2] Prevention and treatment involve maintaining a healthy diet, regular physical exercise, a normal body weight, and avoiding use of tobacco.[2] Control of blood pressure and maintaining proper foot care are important for people with t Continue reading >>
![[metformin - Mechanisms Of Action And Use For The Treatment Of Type 2 Diabetes Mellitus].](https://diabetestalk.net/images/xyXYhIuHdQRSaySB.jpg)
[metformin - Mechanisms Of Action And Use For The Treatment Of Type 2 Diabetes Mellitus].
Zakad Chemii Medycznej, Pomorski Uniwersytet Medyczny w Szczecinie. [email protected] Metformin is widely used for the treatment of type 2 diabetes mellitus. Although this biguanide derivative has been used for more than 50 years, its mechanism of action has not been fully elucidated. In this article we describe the latest achievements concerning the mechanisms of antihyperglycemic action of metformin. They include: decrease of glucose absorption in the small intestine, increase of glucose transport into cells, decrease in the plasma free fatty acid concentrations and inhibition of gluconeogenesis. Activation of AMP-activated protein kinase (AMPK) plays an important role in these processes. The latest discoveries have revealed mechanisms of anti-atherosclerotic, hypotensive and anticancer action of metformin and its impact on vein endothelial function. The pleiotropic actions of metformin include impact on plasma lipid profile, decrease of oxidative stress, and increase in plasma fibrinolytic activity. Although metformin is not metabolized, the latest research has shown that it is actively transported into hepatocytes and renal tubular epithelium, by OCT1 (organic cation transporter 1, encoded by the SLC22A1 gene) and OCT2 (organic cation transporter 2, encoded by the SLC22A2 gene), respectively. However, MATE1 transporter (multidrug and toxin extrusion 1 protein) is encoded by the SLC47A1 gene and facilitates metformin excretion from these cells into bile and urine. Metformin transporter gene polymorphisms may contribute to significant variation in drug response. Further studies of mechanisms of metformin action could contribute to its wider use for the prevention of type 2 diabetes mellitus, cancer, and Alzheimers disease, and for the treatment of type 1 diab Continue reading >>
- International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #59: Mechanisms of insulin signal transduction Part 3 of 8
- Is It Time to Change the Type 2 Diabetes Treatment Paradigm? No! Metformin Should Remain the Foundation Therapy for Type 2 Diabetes
- Glycaemic control in people with type 2 diabetes mellitus during and after cancer treatment: A systematic review and meta-analysis
Drug Treatments For Diabetes Mellitus
The goal of treatments for diabetes mellitus is glycemic control, that is the prevention of hyperglycemia. Chronic hyperglycemia leads to glycation, which is the non-enzymatic addition of sugars to proteins, as well as causing other chemical changes. Ultimately, the various chemical changes due to hyperglycemia are pathological for certain tissues and diabetic complications ensue. The major diabetic complications are listed below. We will discuss these in more detail in Conjoint 402 and 403 when we discuss neural, cardiovascular, and renal physiology. Cardiovascular Disease (heart attack, stroke, peripheral vascular disease) Nephropathy (kidney damage) Retinopathy (blindness) Peripheral Neuropathy (loss of sensation, autonomic dysfunction) Foot Ulcers (amputation) Several large prospective studies have demonstrated that diabetic complications can be significantly reduced by intensive glycemic control. An unfortunate adverse effect of more intensive diabetic therapy is that it increases the risk for hypoglycemia. Glycemic control can be determined through frequent monitoring of blood glucose, but in practice it is measured by measuring HbA1c, or the percentage of glycated hemoglobin. Hyperglycemia causes glycation of proteins, and hemoglobin is a convenient protein to examine since it can be obtained from a simple blood draw. HbA1c (expressed as a percentage) reflects the degree of glycemic control in the previous 4-8 weeks. The American Diabetes Association recommends an HbA1c target of less than 7% for most diabetics. (HbA1c is also now used as a tool for diagnosing diabetes mellitus; see Insulin Resistance). Below are listed major drug treatments for diabetes mellitus that we have discussed in class. Insulin Insulin therapy is necessary for type 1 diabetics because th Continue reading >>
Mechanisms Of Current Therapies For Diabetes Mellitus Type 2
Mechanisms of current therapies for diabetes mellitus type 2 Emory University School of Medicine and Atlanta Veterans Affairs Medical Center, Decatur, Georgia Address for reprint requests and other correspondence: P. M. Thul, Emory Univ. School of Medicine and Atlanta Veterans Affairs Medical Center, Decatur, GA 30033 (e-mail: E-mail Address: [emailprotected] ). The array of medications available for the treatment of hyperglycemia has increased rapidly in the previous decade, and recent investigations have clarified novel mechanisms underlying the antihyperglycemic efficacy of these drugs. This article reviews the mechanisms of action for medications currently approved to treat diabetes mellitus in the United States, with the exception of insulin and its analogs. Finally, it attempts to integrate these mechanisms into the schema of pathophysiological factors that combine to produce hyperglycemia in patients with diabetes mellitus. recent investigations have clarified major aspects of type 2 diabetes mellitus (DM) pathophysiology. As demonstrated by Robert Rizza and colleagues, an oral glucose challenge increases blood sugars in subjects with mild type 2 DM more, and for a longer duration, than subjects without diabetes ( 56 ). Moreover, the expected rise in serum insulin occurs later and remains elevated longer ( 56 ). In addition to this -cell dysfunction, glucagon concentrations remain unsuppressed ( 56 ). In subjects with more pronounced diabetes, glucose levels are greater throughout the challenge, -cell dysfunction is more severe, and normal suppression of glucagon levels is absent ( 56 ). Two additional aspects of pathophysiology among patients with type 2 DM can be observed when subjects are studied during an insulin clamp. In a stepped hyperinsulinemic-euglycem Continue reading >>
Diabetes: Mechanism, Pathophysiology And Management-a Review
Anees A Siddiqui1*, Shadab A Siddiqui2, Suhail Ahmad, Seemi Siddiqui3, Iftikhar Ahsan1, Kapendra Sahu1 Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi (INDIA)-110062. School of Pharmacy, KIET, Ghaziabad U.P. SGC college of Pharmacy, Baghpat(UP) Corresponding Author:Anees A Siddiqui E-mail: [email protected] Received: 20 February 2011 Accepted: 02 May 2011 Citation: Anees A Siddiqui, Shadab A Siddiqui, Suhail Ahmad, Seemi Siddiqui, Iftikhar Ahsan, Kapendra Sahu “Diabetes: Mechanism, Pathophysiology and Management-A Review” Int. J. Drug Dev. & Res., April-June 2013, 5(2): 1-23. Copyright: © 2013 IJDDR, Anees A Siddiqui et al. This is an open access paper distributed under the copyright agreement with Serials Publication, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Related article at Pubmed, Scholar Google Visit for more related articles at International Journal of Drug Development and Research The prevalence of diabetes is rapidly rising all over the globe at an alarming rate. Over the last three decades, the status of diabetes has been changed, earlier it was considered as a mild disorder of the elderly people. Now it becomes a major cause of morbidity and mortality affecting the youth and middle aged people. According to the Diabetes Atlas 2006 published by the International Diabetes Federation, the number of people with diabetes in India currently around 40.9 million is expected to rise to 69.9 million by 2025 unless urgent preventive steps are taken. The main force of the epidemic of diabetes is the rapid epidemiological transition associated with changes in dietary patterns and decreased physical activity a Continue reading >>
Treating Type Ii Diabetes - Pharmacology
- [Voiceover] Type II diabetes receives a lot of attention in the laypress as a public health threat, as it affects about 10% of the global population, and is currently the eighth most common cause of death worldwide. As such, understanding how to treat type II diabetes is very important because if it's treated properly, one can avoid nearly all of the complications of type II diabetes and live a happy and healthy life. Now before we dive into the specific treatments, let's first discuss the glucose regulation pathway as it will help us to better understand the pharmacokinetics or the mechanisms of action for the different treatments of type II diabetes. Now in the center here is the blood glucose level, and as blood glucose levels increase, say after eating a meal, this is sensed by the pancreas, and the beta cells within the pancreas secrete insulin which acts on cells throughout the body to lower the blood glucose level. Then as blood glucose levels decrease, this is also sensed by the pancreas, and then the alpha cells secrete glucagon which acts to raise the blood glucose levels. And one of the mechanisms by which it does so is by promoting the conversion of glycogen to glucose in the liver which is then released into the blood stream. Now diabetes mellitus is a group of disorders that's caused by dysfunction of the insulin pathway resulting in an inability to lower blood glucose levels. And as you can see by this diagram, there are two main steps that must occur for this pathway to work properly. First, insulin must be secreted by the beta cells of the pancreas. Then second, the cells throughout the body must respond to insulin for it to have an effect. And this glucose regulation pathway can be thought of as similar to that of the temperature regulation in a buil Continue reading >>
