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Diabetes Mellitus

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Peter Helli

Diabetes Mellitus Part 1 Diabetes: excessive excretion of urine Mellitus: disorder of carbohydrates, fat and protein metabolism due to insulin deficiency Prevalence of Diabetes: - The older the adult, the increased prevalence - Increased risk of heart disease, stroke, kidney disease, blindness, amputation, erectile dysfunction, and reduced quality of life Etiology Type 1 DM: characterized into two groups Autoimmune type 1A: • Autoimmune mediated specific loss of beta cells in the pancreatic islets Langerhans • Accounts for 90-95% of type 1 diabetes cases • As a whole it includes cases of diabetes that are primarily the result of beta cell destruction which leads to absolute insulin deficiency and is prone to ketoacidosis • This is believed to be a result of a genetic-environment interaction • Genes: o MHC genes on chromosome 6encode leukocyte antigens HLA-DQ and HLA-DR o Some leukocyte antigens are known to decrease the risk of developing type 1 diabetes such as HLA-DR2 o Chromosome 11- insulin gene regulating beta cell replication and function, there is also an insulin gene that regulates beta cell replication and function on chromosome 11 • There are many polymorphisms of multiple genes that have been identified as influencing the risk of type 1a diabetes • Autoantibodies related to beta cell destruction include: insulin autoantibodies, islet cell autoantibodies, antibodies directed at other islet autoantigens (glutamic acid decarboxylase-GAD and tyrosine phosphatase IA-2) • Environmental factors also interact with genes: drugs and chemicals; Nutritional intake, such as bovine milk linked to type 1 diabetes; viruses, 40% of individuals with congenital rubella infection develop type 1 diabetes later • Seems to be a seasonal distribution with more new cases reported in the fall and winter in the Northern hemisphere, this proposes the idea that there is a gene-environment interaction which causes type 1a diabetes to manifest • There are some individuals with type 2 diabetes that actually fall into this type 1a category instead because of the mediated specific loss of beta cells in the islets of Langerhans- Latent autoimmune disease in adults or LADA • Usually type 1 diabetes occurs in childhood, peaking at 12 years Idiopathic Type 1B (Non-immune type 1 diabetes): • No evidence of autoimmunity, the etiology is unknown • It accounts for less than 10% of those with type 1 diabetes • There is a strong genetic component to type 1B diabetes, most affected are individuals from African or Asian descent • Individuals have varying degrees of insulin deficiency, it can come and go, which leads to episodic ketoacidosis Etiology Type 2 DM: • Characterized by hyperglycemia, insulin resistance and relative insulin deficiency • Range from predominant insulin resistance with relative insulin deficiency to a predominant secretory defect with insulin resistance • Also thought to involve an environmental-genetic interaction • 15-25% of first degree relatives of people with type 2 diabetes will develop either impaired glucose tolerance or diabetes • Genes: genetic defects of beta cell function; genetic defects in insulin synthesis, secretion and action • Variance of genes have been identified for increasing the risk of type 2 diabetes, many of them fall into the category of genetic defects, beta cell function, genetic defects in insulin synthesis, secretion and action, others include genes that code proteins • Risk Factors: include age, obesity, hypertension, physical inactivity and family history • + metabolic syndrome high risk of developing type 2 diabetes and associated cardiovascular complications • It occurs mostly in adults, however increasing prevalence in children as childhood obesity rates climb • Canadian aboriginal children are particularly effective Gestational Diabetes Mellitus: • Defined as any degree of glucose intolerance with onset or first recognition during pregnancy • Pre-gestational diabetes refers to pregnancy in persons with pre-existing diabetes • Exact etiology of glucose intolerance is unknown, however a combination of insulin resistance and impaired insulin secretion are most definitely contributing factors • Risk factors include: older age, family history, history of glucose intolerance, obesity, membership in certain ethnic or racial groups, history of poor obstetric outcomes, and infant weighing greater than 9 pounds • Diagnosis is made based on the gestational diabetes screen, which is a 50 gram glucose load, followed by a plasma glucose level one hour later • Untreated gestational diabetes, leads to increase maternal, perinatal morbidity Other: • Specific genetically defined forms of diabetes include genetic defects of beta cell function and genetic defects in insulin action • Maturity onset diabetes of the young (MODY): these individuals presented at a young age, have mild disease due to beta cell dysfunction, with some insulin production and inherit the disease thru autosomal dominant transmission o There is normal insulin sensitivity in individuals with MODY o MODY type 2 and 3 stand for most cases of MODY • Diabetes associated with other diseases/disorders • Diabetes induced by infections, drugs or chemicals Why would someone with Cushing’s disease have a higher risk of developing diabetes? Cortisol plays a role in glucose in the blood Glucose Metabolism: - Glucose is a 6 carbon molecule, efficient for fuel, breaks down into CO2 and H2O when metabolized in the presence of oxygen - The brain and nervous system rely almost solely on glucose as a fuel source - Other tissues and organ system can use other sources for fuel such as fatty acids and ketones - The brain is not able to synthesize glucose, or store any as well, therefore a continuous supply of glucose is needed to maintain normal cerebral function - FBG (fasting blood glucose) is tightly regulated between 4.4-5.0 mmol/L in non-diabetic persons - Insulin is secreted by beta cells in response to rising blood glucose levels - After a meal is ingested approx. 2/3 glucose is stored in the liver as glycogen - Btw meals the liver releases glucose by breaking down glycogen in a process called glycogenolysis to maintain normoglycemia (normal glucose levels) - Once the liver and skeletal muscles are saturated with glycogen, additional glucose is converted into fatty acids by the liver and then stored as triglycerides in adipose tissue - The liver also synthesizes glucose form a non-carbohydrate source like amino acids and lipids in a process called gluconeogenesis Protein Metabolism: - Proteins essential for the formation of all body structures - Amino acids are the building blocks of proteins - Limited capacity for the storage of excess amino acids, most stored amino acids are stored in body proteins - Amino acids not needed for protein synthesis are converted to fatty acids, ketones, or glucose and then stored or used as metabolic fuel - Amino acids are broken down from proteins and are used as a major substrate for gluconeogenesis when metabolic needs exceed food intake Fat Metabolism: - Is the most efficient fuel storage - 30-35% of calories obtained from fat in a normal Canadian diet - 55% are obtained from carbohydrates and 15% from protein - Many carbohydrates consumed in diet converted to triglycerides and stored in adipose tissue - Triglyceride= 3 fatty acids linked by a glycerol molecule - LIPASE breaks down triglycerides into its four components when fat is required for fuel - Glycerol used in glycolysis or to produce glucose - Fatty acids transported to tissues to be used for energy can be used in almost all body cells EXCEPT:  The brain  Nervous system  Red blood cells - The liver converts left over fatty acids into ketones and releases them into the bloodstream What happened when large amounts of ketones (organic acids) are released into the blood stream? Ketoacidosis! Putting it all together: • The brain requires a constant supply o
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