What is Diabetes mellitus and its types

In diabetes mellitus, plasma blood glucose increases, leading to hyperglycemia, characterizing the clinical syndrome. It has many causes

There are two most common types of diabetes Type 1 and Type 2

Autoimmune destruction of insulin-producing cells (β cells) in the pancreas generally causes Type 1 diabetes, resulting in marked insulin deficiency.

In Type 2 diabetes, reduced sensitivity to the action of insulin and an inability to produce sufficient insulin to overcome this ‘insulin resistance’ characterize the condition.

Hyperglycaemia causes both acute and long-term problems.

High glucose levels and insufficient insulin acutely lead to pronounced symptoms, metabolic decompensation, and necessitate hospitalization.

Persistent high blood sugar levels cause diabetes-specific ‘microvascular’ complications, impacting the eyes (retinopathy), kidneys (nephropathy), and feet (neuropathy).


About 1 million islets, scattered throughout the exocrine parenchyma, comprise the normal adult pancreas.

β cells within the core of each islet produce insulin, surrounded by a cortex of endocrine cells that produce other hormones, including glucagon (α cells), somatostatin (δ cells), and pancreatic polypeptide (PP cells).

Glucose enters the cell via a glucose transporter (GLUT1 or GLUT2).

Glucose then enters glycolysis, and subsequent oxidative phosphorylation in the mitochondria results in a rise in intracellular adenosine triphosphate (ATP).

This ATP acts to close the KATP channel (which consists of four KIR6.2 subunits and four SUR1 subunits). This leads to membrane depolarisation.

The rise in membrane potential results in calcium influx due to opening of a voltage-gated calcium channel. The increase in intracellular calcium prompts the fusion of insulin secretory vesicles with the cell membrane, resulting in the secretion of insulin.

Stimuli like glucagon-like peptide-1 (GLP-1) or gastric inhibitory polypeptide (GIP) activate G-protein-coupled receptors, leading to an increase in cyclic adenosine monophosphate (cAMP) levels, thereby enhancing insulin secretion.


Both common types of diabetes involve a complex interplay between environmental factors and genetic predisposition to determine the individuals who manifest the clinical syndrome and when it emerges.

However, the underlying genes, precipitating environmental factors and pathophysiology differ substantially between type 1 and type 2 diabetes.

Previously termed ‘insulin-dependent diabetes mellitus’ (IDDM), Type 1 diabetes invariably requires replacement therapy due to insulin deficiency.

Type 2 diabetes, once known as ‘non-insulin-dependent diabetes mellitus’ (NIDDM), is characterized by patients maintaining the ability to secrete insulin, with measured insulin levels frequently surpassing those found in individuals without diabetes.

In Type 2 diabetes, affected individuals usually experience impaired sensitivity to insulin (insulin resistance) and can typically be treated initially without requiring insulin replacement therapy.

Overeating, especially when combined with obesity and under-activity, associates with Type 2 diabetes.

The Type 2 diabetes is more common in middle-aged and older individuals

Type 1

It generally consider Type 1 diabetes as a T-cell-mediated autoimmune disease.

It involves destruction of the insulin-secreting β cells in the pancreatic islets

The pathology in the pre-diabetic pancreas is characterised by an inflammatory lesion within islets, ‘insulitis’ with infiltration of the islets by mononuclear cells containing activated macrophages, helper cytotoxic and suppressor T lymphocytes, natural killer cells and B lymphocytes.

Autoimmunity in type 1 diabetes is identified by the presence of autoantibodies to islet and/or β-cell antigens.

Islet cell antibodies can be present long before the clinical presentation of type 1 diabetes, and their detection can be useful in confirming a diagnosis of type 1 diabetes

Type 2

Healthcare providers make a diagnosis of Type 2 diabetes by excluding Type 1 diabetes and other types of diabetes; it is highly heterogeneous.

At the onset, insulin resistance prompts heightened insulin secretion to uphold standard blood glucose levels.

Nonetheless, in susceptible individuals, the pancreatic β cells fail to meet the escalating demand for insulin, resulting in the gradual onset of insulin deficiency.

While some individuals acquire diabetes in youth, primarily due to insulin resistance linked with obesity and ethnicity, others, particularly older patients, develop the condition despite not being obese and may exhibit more significant β-cell deterioration.

Resistance to insulin action is thought to cause a cluster of conditions including Type 2 diabetes and its pre-diabetes antecedents.

Thus, people with type 2 diabetes often have associated disorders including hypertension, dyslipidaemia (characterised by elevated levels of small dense low-density lipoprotein (LDL) cholesterol and triglycerides, and a low level of high-density lipoprotein (HDL) cholesterol), non-alcoholic fatty liver disease and, in women, polycystic ovarian syndrome.

This cluster has been termed the ‘insulin resistance syndrome’ or ‘metabolic syndrome’, and is much more common in individuals who are obese.

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