Diabetes Mellitus: Metabolic Syndrome and Role of Incretins!

METABOLIC SYNDROME AND INCRETIN EFFECT

METABOLIC SYNDROME:

"Insulin resistance has been associated with a number of other cardiovascular risks, including Abdominal obesity, Hypertension, Dyslipidemia, Hypercoagulation, and Hyperinsulinemia. The clustering of these risk factors has been termed as Metabolic syndrome."

The most widely used criteria to define metabolic syndrome were established by the National Cholesterol Education Program Adult Treatment Panel III Guidelines.

INCRETIN EFFECT

Incretins: are a group pf metabolic hormone that stimulate a decrease in blood Glucose levels.
Incretin hormones are: GLP-1, GIP.
Incretins are gut hormones that are secreted from entero-endocrine cells into blood within minutes after eating (present in GIT, Stomach, and Pancreas).
A great deal of research is occurring today to develop compounds that enhance the incretin effect, either by mimicking its action or y enabling incretin hormones, to remain physiologically active for longer periods of time.

As early as the late 1960s, Perley and others observed that insulins response to oral glucose exceeded that of intravenous glucose administration. It was conducted that factors in the gut, or incretins affected the release of insulin after a meal is consumed.

When nutrients enter the stomach and intestine, incretin hormones are released which stimulates Insulin secretion.
GLP-1 & GIP are two major incretin hormones; with GLP-1 being studied the most.

GLP-1 is secreted by the L-cells of the ileum and colon primarily. GLP-1 secretion is caused by the endocrine and neural signals started when nutrients enter the gastrointestinal tract. A glucose dependent release if insulin occurs, and the dipeptidyl peptidase (DDP-4) enzyme cleaves GLP-1 rapidly to an inactive metabolite. Other glucose lowering effects of GLP-1 include suppression of glucagon, slowing gastric emptying, and increasing satiety.

GIP is secreted by the K-cells.

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Diabetes Mellitus: Types!

TYPES OF DIABETES MELLITUS 1. TYPE1 DM Type 1 DM is usually diagnosed before age 30 years, but it can develop at any age. T1DM is an autoimmune disease in which insulin producing B-cells are destroyed. The presence of Human Leucocyte Antigens (HLAs ) is associated with the development of T1DM. In addition, these individuals often develop Islet cell antibodies , Insulin Autoantibodies or Glutamic Acid decarboxylase autoantibodies . At the time of development of diagnosis of T1DM, it is usually believed that most of the patients have 80-90%loss of beta cells. The remaining beta cells function at the diagnosis creates a " HONEYMOON PERIOD" during which the blood glucose levels are easier to control, and smaller amounts of insulin are required. after this, the remaining beta cells function is completely lost, and the patients become completely deficient of insulin and hence require exogenous insulin. 2. TYPE1.5 DM: Also referred as Latent autoimmune diabetes in Adults (LAD)

Diabetes Mellitus: Pharmacotherapy- Gliptins and a-Glycoside Inhibitors!

PHARMACOTHERAPY: Medications classifications include: Sulfonyl Urea's Nonsylfonylurea Secretagogues (a-Glinides) Biguanides Thiazolidinediones a-Glucosidase Inhibitors Dipeptidyl Peptidase-4 Inhibitors (Gliptins) Sodium-glucose co-transporter (SGLT) Inhibitors Central-Acting Dopamine Agonists Bile Acid Sequestrants Insulin therapy 5. a-GLUCOSIDASE INHIBITORS Acarbose and Miglitol are a-glucosidase inhibitors currently approved in the United States. Mechanism of Action: An enzyme that is along the brush border of the intestine cells called a-glucosidase; breaks down the complex carbohydrates into simple sugars, resulting in absorption. The a-glucosidase inhibitors work by delaying the absorption of carbohydrates from the intestinal tract, which reduces the rise in postprandial glucose levels. Therapy: As a monotherapy , a-glucosidase inhibitors primarily reduce post-prandial glucose excursions. Clinical Use: FPG concentrations have been decreased by 40-50mg/dL and A1c level

GASTRO-ESOPHAGEAL REFLUX DISEASE (GERD)!

MANAGEMENT OF GASTRO-ESOPHAGEAL REFLUX DISEASE "GERD refers to the endoscopically determined esophagitis or endoscopy-negative reflux disease" . "GERD is the term used to describe any symptomatic clinical condition or histopathological alteration resulting from episodes of reflux of acid, pepsin and occasionally, bile into the esophagus from the stomach". Patients with uninvestigated "reflux-like" symptoms should be managed as patients with uninvestigated dyspepsia. There is currently no evidence that H.pylori should be investigated in patients with GERD. Symptoms: Heartburn is the characteristic symptom of GERD. Acid regurgitation Dysphagia Belching Upper abdominal discomfort Bloating and postprandial fullness Chest pain Hoarseness Cough Complications include: Esophageal ulceration Formation of specialized columnar-lined esophagus at the gastro-esophageal junction known as Barretts Esophagus . Mechanism of Acid Reflux: The mechanism of acid reflux is mu

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