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How GLP 1 works:
- The Incretin Effect: GLP-1 amplifies the body’s natural insulin response following meals. This discovery explained why people respond differently to glucose ingested versus glucose injected, as GLP-1 is active in response to oral intake.
- Glucagon Suppression: GLP-1 lowers glucagon secretion, further improving blood sugar control by preventing unnecessary glucose release from the liver.
- Gastric Emptying: GLP-1 slows down gastric emptying, or how quickly food leaves the stomach. This action increases feelings of fullness, aiding weight management efforts.
- Neuroprotective Effects: Emerging evidence suggested that GLP-1 might have protective effects on brain cells, sparking interest in its potential for treating neurodegenerative conditions like Alzheimer’s disease.
STEP 2A: PERSONALIZED WELLNESS PLAN
- echanism of Action:
- a synthetic analog of glucagon-like-polypeptide 1 (GLP-1) that is resistant to breakdown by DPP-IV. It has multiple actions including:
- potentiation of glucose-mediated insulin secretion
- mechanisms identified:
- increased β-cell proliferation, resulting in an increase β-cell mass (Fusco et al, 2017)
- stimulation of insulin biosynthesis at the translational level, helping to maintain β-cell insulin stores and secretory capacity (Baggio & Drucker, 2007)
- because the GLP-1 effect is glucose-dependent (there is more insulin release when glucose levels are elevated, but less effect when glucose levels are normal), GLP-1 agonists have a lower risk for producing hypoglycemia compared to sulfonylureas (that chronically stimulate insulin release, independent of glucose concentration)
- mechanisms identified:
- potentiation of glucose-mediated insulin secretion
- a synthetic analog of glucagon-like-polypeptide 1 (GLP-1) that is resistant to breakdown by DPP-IV. It has multiple actions including:
STEP 2B: Nutritional Meal Plans and Supplements
STEP 2B: Nutritional Meal Plans and Supplements
STEP 2B: Nutritional Meal Plans and Supplements
- slowed gastric emptying
- GLP-1 agonists stimulate GLP-1 receptors in the CNS including vagal efferent fibers in the brainstem. The resulting increase in vagal toe inhibits gastric emptying and gastric acid secretion, subsequently resulting in a delay of gastric emptying, and reduction of glucose absorption (Shaefer et al, 2015).
- The reduction of parasympathetic tone can undergo tachyphylaxis with chronic GLP-1 stimulation.
- reduction in liver fat content
- liver fat accumulation is correlated with several metabolic disturbances including low HDL and elevated triglyceride levels(Tushuizen et al, 2006).
IMPLEMENTATION AN FOLLOW THROUGH
STEP 2B: Nutritional Meal Plans and Supplements
STEP 2B: Nutritional Meal Plans and Supplements
- suppression of postprandial glucagon release
- Evidence indicates that stimulation of pancreatic α cells by GLP-1 increases their glucose sensitivity, resulting in less glucagon release at any glucose level (Baggio & Drucker, 2007).
- decreasing glucagon production reduces the amount of endogenous glucose produced by the liver (see Figure). This in turn reduces the amount of insulin the body needs, ultimately resulting in reduced hyperglycemia and improved control of glucose levels.
- centrally-mediated loss of appetite & increased thermogenic activity
- GLP-1 receptors are found in regions of the hindbrain and hypothalamus that regulate feeding behavior
- Centrally mediated GLP-1 effects include:
- reduction of food intake - resulting in weight loss due to reduced caloric intake
- activation of sympathetic pathways in the dorsomedial hypothalamus (DMH) and ventromedial nucleus of the hypothalamus (VMH) that increase neuronally mediated thermogenic activity of brown adipose tissue (BAT) resulting in increased energy expenditure with associated weight loss
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