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Diabetes Pathophysiology

Diabetes is projected to be the 7th preeminent cause of death in America by 2030.  There are two main types of diabetes: type-1 diabetes and type-2 diabetes. Type-1 diabetes, most clinically and notoriously known as insulin-dependent juvenile-onset diabetes mellitus, transpires when the pancreas lacks or possesses defective β-cells.  This is exceedingly consequential; because, the β-cells act as individual machineries, which manufactures insulin, essentially lowering blood glucose levels.  This notable process transpires in the Islets of Langerhans of the pancreas, which are disseminated minute clusters of cells.  Figure 1 illustrates Islets of Langerhans, which comprise alpha (α), beta (β), and delta (△) cells.  These cells secrete peptide hormones, which regulate blood glucose levels directly and indirectly.  The two direct blood glucose regulators are α-cells, which secrete glucagon, and β-cells, which secrete insulin; whereas, △-cells, which secrete somatostatin, are indirect regulators of blood glucose, essentially inhibiting the production of insulin and glucagon.

Figure 1: A single Islet of Langerhan comprising α-cells (dark blue), β-cells (light blue), and △-cells (purple) surrounded by pancreatic acini and red blood cells.

 

Furthermore, the chromaffin cells of the adrenal medulla and the zona fasciculata of the adrenal cortex produce glucose regulating stress hormones known as epinephrine and cortisol, respectively.  However, the preeminent hormones related to type-1 diabetes are insulin and glucagon.  After the ingestion of a meal, glucose levels are elevated, which induces a progressive release of insulin; and, consequently, blood glucose levels are lowered.  In contrast, scarce quantities of glucose in the blood induce a progressive release of glucagon, essentially elevating blood glucose levels.  The progressive release of insulin exclusively, after the ingestion of a meal, is habitually seen in the indefectible β-cells of non-diabetics; whereas, defective β-cells of type-1 diabetics fail to synthesize any or secrete sufficient quantities of insulin.

 

Thus, daily synthetic insulin or exogenous insulin injections are therapeutically essential in managing type-1 diabetes.  However, if insulin cannot function to its full potential, then medical nutrition therapy in combination with synthetic insulin injections are imperative in managing type-1 diabetes. It is consequential to note that type-1 diabetes is commonly seen in children and adolescents.  The three classic trio of symptoms that usually transpire are polydypsia (excessive thirst), polyphagia (increased appetite), and polyuria (increased urination).

 

Type 2-diabetes, most clinically and notoriously known as non-insulin-dependent maturity-onset diabetes mellitus, is the preeminent type of diabetes diagnosed in the United States of America.  Although type-2 diabetes is commonly seen in adults, recent literature denotes that there has been a substantial occurrence in overweight and obese children and adolescence.  Type-2 diabetes transpires when the cells (adipose, muscle, and liver) that habitually absorb and store glucose fail to respond properly to insulin, notoriously known as insulin-resistance.  Now many individuals may figuratively compare insulin resistance to antimicrobial resistance; however, both forms of resistance are quite different from one another.

 

Antimicrobial resistance refers to a specific strain of pathogenic bacteria becoming resistant to an antimicrobial agent, such as soap, laundry detergent, toothpaste, ect.  While, the susceptible cells of the pathogenic bacteria die, the resistant cells unabatedly proliferate. Antimicrobial resistance is induced by a pathogenic strain having continuous contact with an antimicrobial agent; whereas, insulin resistance is induced by insulin impotently binding to an insulin-receptor, essentially inducing primarily the muscle cells to become unresponsive to insulin.  Consequently, a higher quantity of insulin is released by the β- cells to succor glucose absorption.  However, a high demand for insulin is not sustainable and exhausts the β-cells, essentially inducing β-cell lysis.  In other words, the binding of insulin to an insulin-receptor relationship is the only way, in which glucose can enter a cell.  Figure 2 illustrates a normal cell and an insulin resistant cell.

Figure 2: The top photo illustrates a normal cell, in which insulin binds to the insulin-receptor enabling glucose to enter the cell; whereas, the bottom photo illustrates a myriad of insulin and glucose remaining in the bloodstream induced by a blockage of lipids.

 

Imagine this process as a key, lock, piece of gum, and an old man named Mr. Bean.  In a normal cell, the key (insulin) unlocks the door, so that Mr. Bean (glucose) can enter the cell.  In an unresponsive insulin resistant cell, the key (insulin) cannot unlock the door; because, an eight year old girl placed gum (lipid) inside of the lock.  Without a key (insulin) being able to open the door, Mr. Bean (glucose) will remain locked outside of his house.  This is an exemplary explanation of how intramyocellular lipids derived from dietary lipids induce insulin resistance, which induces type-2 diabetes.

 

A plethora of research denotes that intramyocellular lipids serve as a preeminent marker for insulin resistance.  A whole foods, low-fat, plant-based diet can reverse the deleterious effects of insulin resistance making synthetic or exogenous insulin administration redundant for the management of type-2 diabetes.  It is imperative to note that prediabetes, which usually possesses no symptoms, can induce type-2 diabetes; and, the symptoms of type-2 diabetes are similar to type-1 diabetes.  Please enjoy the plethora of research below that supports the ingestion of a whole foods, low-fat, plant-based diet, which serves as a therapeutic approach in managing type-1 diabetes and reversing type-2 diabetes.

 

-Anastasia L. Floyd, Nutrition For a Lifetime’s Student Assistant

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