Polypeptide hormone secreted by the alpha cell of the pancreatic islets.

A 29 amino acid peptide hormone that is counterregulatory to insulin, stimulating hepatic glucose production, there by increasing plasma glucose levels.

Released by alpha cells in response to hypoglycemia or any event requiring extra glucose, like exercise.

Regulates the actions of insulin and maintains serum glucose levels.

Normal glucose homeostasis depends on a balance secretion of glucagon and insulin from pancreatic alpha and beta cells, respectively, in a regulated multi loop feedback system.

Important in glucose homeostasis and diabetes pathophysiology

Activates hepatic glycogenolysis.

Following a meal, high glucose levels stimulate the pancreas to increase insulin.

It is a counterregulatory hormone released from pancreatic alpha cells during hypoglycemia, increasing blood glucose.

Glucagon has potent catabolic effects that stimulates adipose lipolysis,  reduces food, intake, slows gastric emptying, and increases energy expenditure.

Stimulates the liver to breakdown glycogen, activates the conversion of amino acids into glucose and breaksdown triglycerides into fatty acids.

The hormone glucagon signals the breakdown of the triglycerides by hormone-sensitive lipase to release free fatty acids to be used as an energy source.

Glucagon acts on the liver to trigger glycogenolysis and gluconeogenesis.

Promotes glucose synthesis via glucogenesis, inhibits further glycogen formation, immobilizes export of glucose into the circulation

Insulin acts as a glucose depositing and anabolic hormone, whereas glucagon is glucose mobilizing and catabolic.

When plasma glucose levels fall too low, the pancreas releases glucagon.

Primarily stimulated by hypoglycemia.

Stimulated by amino acids, epinephrine.

Release inhibited by insulin and hyperglycemia.

Elevated levels associated with hyperglycemia.

While hyperglycemia decreases glucagon secretion, evidence exists that abnormal secretion of glucacon from alpha cells contributes to metabolic derangements in diabetes, and many diabetics with hyperglycemia also have elevated glucagon levels.

Pathophysiology of type two diabetes includes aberrant secretion of glucagon, resulting in the elevated glucagon concentrations in both the fasting state and after a meal.

It is a consideration that excess glucagon, rather than an insulin deficiency, may be the primary defect in diabetes.

Activates phosphorylase to cause glycogenolysis.

Increases uptake of amino acids by the liver for gluconeogenesis.

Plays a role in lipid metabolism, influences food intake, affects bodyweight, promotes autophagy, and has pleiotropic effects on the cardiovascular system.

Does not effect muscle glycogen stores.

Promotes ketone formation from acetyl-CoA produced by hepatic oxidation.

Acts by generation of cAMP.

Exerts opposite effects of insulin on blood glucose.

Elevates blood glucose levels by inhibiting glycogen synthesis and enhancing formation of glucose from noncarbohydrate sources, such as proteins and fats.

Increases hydrolysis of glycogen to glucose (glycogenolysis) in liver in addition to accelerating hepatic glycogenolysis and lipolysis in adipose tissue.

Increases force of contraction in heart and has a relaxant effect on GI tract.

Usual dose of 1 mg (1 U) IV/IM/SC used to treat hypoglycemia.

Glucagon levels moderated by antidiabetic medications dipeptidyl peptidase-4 inhibitors and glucagon-like peptide-1 receptor agonists, both which suppress glucagon secretion.

Sulfonylureas,insulin, amylin mimetics, and sodium-glucose cotransporter 2 inhibitors (SGLT2).

Glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors reduce plasma glucagon concentrations benefiting patients with type 2 diabetes who have excessively high post meal blood sugars, even if they consume very few carbohydrates.

Sodium cotransporter-2 inhibitors (SGLT-2) increase loss of glucose in the urine and produce an increase in glucagon.

Combining SGLT-2 inhibitors with incretin mimetics reduces glucagon levels and reduces hyperglycemia and HbA1c.

Dipeptidyl-peptidase -4 inhibitors and glucagon-like peptide-1 receptor agonists,decrease glucagon secretion, resulting in amelioration of inappropriately high glucagon concentrations characteristic of type two diabetes and improvement of the insulin: glucagon ratio.

Combining SGLT-1 inhibitors with DPP-4 inhibitors or/and GLP-1 receptor agonists can decrease elevations in glucagon.

Nasal glucagon approved for the treatment of hypoglycemia without injection (Baqsimi).

Baqsimi is an intra-nasal powder indicated for severe hypoglycemia in patients with diabetes who are aged 4 years or older.

Baqsimi increase his glucose levels at least 70 mg/deciliter or a 20 mg/dL or higher increase in plasma glucose from nadir within 30 minutes.

Adverse events with adverse events include nausea, vomiting, headache, respiratory tract irritation, itchy nose, throat and eyes.

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