DIABETES MELLITUS: The Pathophysiology of DM

There’s an old saying about “writing what you know.” Keeping that in mind, I’ve decided to write a series of blogs about diabetes mellitus (DM) since I have Type 2 DM. Actually, I suspect I really have Type 1.5, AKA LADA. You may not even know the terms Type 1.5 or LADA, as presently, there is no official recognition or code number for Type 1.5. However, before we can even discuss code assignments for any type of diabetes, there’s lots to know about diabetes as a disease. Future blogs will delve into “all things diabetes,” including gestational diabetes, other manifestations/complications of diabetes, and assigning ICD-10-CM codes; for today, let’s focus diabetes as a disease.

Let’s begin with Types 1 and 2 DM. These types of diabetes are polygenic, which means they are related to changes/defects in multiple genes in the human body. As we learned in biology classes, genes provide instructions for making proteins within a cell. When it comes to polygenic diabetes, mutated genes interfere with the body’s ability to produce insulin and effectively manage blood glucose.


Type 1 diabetes is caused by an impaired immune system that begins attacking and destroying insulin-producing pancreatic beta cells. Once these cells are destroyed, the pancreas cannot produce insulin. Exactly why the immune system turns on itself is unknown; it’s believed genetics and environmental factors like exposure to viruses are involved. Type 1 DM is an autoimmune disease and frequently occurs concomitantly with other autoimmune diseases such as celiac disease.


Type 2 diabetes is caused by insulin resistance. The body continues to produce insulin, but cannot use it efficiently, meaning glucose accumulates in the bloodstream. It is most often caused by a combination of lifestyle factors along with genetic and environmental factors.


Type 1.5 – aka LADA (Latent Autoimmune Diabetes of Adults) is sometimes called “double diabetes” because adult patients have aspects of both Types 1 and 2.


Going back to biology lessons, remember that humans typically have two copies of most genes – one from each parent. Some forms of DM are cause by a mutation of a single, monogenic, gene. Occurring in roughly 1-4% of all U,S, diabetics, this mutation can be inherited from one or both parents; there are instances where it’s occurred spontaneously. Monogenic mutations interfere with the pancreas’ ability to produce insulin. Neonatal DM and MODY – Maturity-Onset Diabetes of the Young – are the two most common forms of monogenic DM. MODY typically first appears in adolescence/early adulthood. It’s estimated to occur in 2% of all U.S. diabetics ages 29 and younger. Easily confused with both Types 1and 2 DM, MODY presents in several different ways, depending on the actual gene mutation. (See Graphic # 1 for further information.) Genetic testing is often indicated if diabetes is diagnosed in a young adult who exhibits atypical diabetic symptoms such as autoantibodies, obesity, and other metabolic features. Testing would also be indicated in people with stable, mild-fasting hyperglycemia, especially in the absence of obesity.


Over the years, researchers have fine-tuned how diabetes is classified. Terms like “juvenile-“ and “adult-onset” gave way to “insulin-dependent/non-insulin-dependent,” and even “insulin-requiring.” The terms “Type 1/Type 2” were coined in the 1990s. “LADA” and “Type 1.5” came about in the late 1990s.  


Wow! It’s evident that there’s a lot to take in when it comes to understanding DM! Hopefully, this first blog in the series on diabetes has increased your clinical understanding of diabetes. Next time, we’ll begin looking at assigning ICD-10-CM codes; future blogs will delve into OGCR and CDI implications in addition to proving new information on diabetes and how it is both classified and treated.









70% of MODY cases are caused by this gene. It causes the pancreas to lower the amount of insulin it produces. Diabetes usually develops in adolescence or early 20s.

Insulin is not usually required, though patients may need small amounts of sulfonylureas.


Not as common as other forms of MODY, those with this genetic mutation most likely weighed 9 or more pounds at birth. They also have had a treatment-requiring episode of hypoglycemia at or soon after birth.

Usually treated with sulfonylureas, but may progress to requiring insulin.


In addition to causing MODY, this genetic mutation has been associated with other problems such as renal cysts (which can often be detected in utero), uterine abnormalities, and gout. Diabetes tends to develop later; this genetic mutation also carries a risk of complications of diabetes.

Insulin treatment is usually necessary, as is following a proper diet and regular physical exercise.


This gene assists in recognizing how high the blood glucose is in the body. When it doesn’t work properly, blood glucose levels rise higher than they should be. Typically, the glucose levels are only slightly elevated and it is usually symptomless. This type of MODY is more often noticed through routine lab tests, such as those performed during pregnancy.

Generally not treated.


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