Hormones Involved in Blood Glucose Homeostasis: 

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Pancreatic Islet Hormones

Glucagon:

    Cellular uptake of glucose (and resulting decrease in blood glucose) stimulates secretion of glucagon from the pancreatic islets

      Glucagon (in the presence of cortisol...discussed later) acts in diametrically opposite fashion to insulin:

        decreases cellular uptake of glucose

        increases synthesis (from stored glycogen and from amino acids) and release of gl;ucose from the liver

        increases the breakdown of fats and the formation of ketones and ketoacids (which are potential energy sources)

    Glucagon secretion is also stimulated by stress (i.e. the presence of diabetogenic hormones such as cortisol, epinephrine (adrenaline) and other hormonal signals ( originating in the gastrointestinal tract) triggered by the ingestion of food.

    Glucagon, in turn, stimulates insulin secretion. Putatively, the delicate balance between the antagonistic effects of the two hormones results in fine tuning the steady-state levels of blood glucose, and thus, prevents wide fluctuations

    Glucagon secretion decreases when blood sugar is elevated BUT this inhibition is insulin-dependent! In the absence of insulin, glucagon persists, and hyperglycemia (high blood sugar) is exacerbated (by low insulin AND by high glucagon levels)

Somatastatin

    Synthesis is stimulated by the same factors that stimulate insulin and by gastrointestinal digestive processes

    Inhibits glucagon and insulin responses

    Glucagon stimulates the production of somatastatin

    Effects to inhibit or minimize indefinite "cycling" or glucagon-insulin

Polypeptide Hormone

    Reduces glycogen stores (in liver) but without increasing blood sugar levels

    Secretion is decreased by high blood sugar and by somatastatin

Non-Pancreatic Hormones

The Counter-Current Hormones **

    (see potential consequences of prolongued stimulation of these)

    Normally, in the presence of hypoglycemia (i.e. low blood sugar) the "counter-current" hormones (those that quickly antagonize a rapid drop in blood sugar) are triggered. These are:

      Epinephrine ("Adrenaline")/Norepinephrine: these neurotransmitters act on the liver to effect release of glucose into the bloodstream

      Growth Hormone ("anti-insulin"):

        decreases the uptake and utilization of glucose by cells (thus antagonizing the effects of insulin)

        potentiates the breakdown of fat to ketones and ketoacids (see discussion of diabetic ketoacidosis in "Diabetes" web page in previous web browser window)

        stimulates the synthesis and release of glucose from the liver

      Cortisol/Corticosteroids:

        These are required for glucagon to facilitate it's effects to elevate blood sugar
        (NOTE: 
        a deficiency in cortisol...e.g. in hypoadrenocorticism [Addison't Disease] can result in acute collapse from hypoglycemia (glucagon needs cortisol to maintain blood sugar levels!!!))

        Facilitate release of glucose from the liver

        Decrease utilization of glucose by many tissues

        Promote ketone and ketoacid synthesis

      Non-physiological Effectors of Blood Glucose:

        Other mediators of (substances, drugs) are potentially diabetogenic (promote diabetes). These include reproductive hormones (e.g. progesterone), various drugs/medications, neurologic disease, (affecting direct stimulation of the pancreas from the autonomic nervous system).

**While effective in preventing hypoglycemia, prolongued exposure to these hormone results in hyperglycemia (high blood sugar); hyperglycemia, in turn, stimulates insulin secretion. Chronic stimulation of insulin secretion will eventually "exhaust" ß-cells and this will result in Glucose Toxicity (discussed with Diabetes (previous browser window)...and, potentially...IDDM!!!!

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