Oskar Minkowski and the Discovery of the Pancreas’ Role in Diabetes

In 1889, German physiologist Oskar Minkowski, in collaboration with Joseph von Mering, made a pivotal discovery that transformed the scientific understanding of diabetes. Through experiments on dogs, they found that removing the pancreas induced severe diabetes, marked by elevated blood sugar levels and sugar in the urine. This groundbreaking observation demonstrated, for the first time, the critical role of the pancreas in metabolism and glucose regulation.

Minkowski proposed that the pancreas produced a substance essential for controlling blood sugar levels. Though the exact nature of this substance was unknown at the time, it was later identified as insulin by researchers Frederick Banting and Charles Best in 1921. Insulin is now recognized as a hormone crucial for glucose uptake and utilization by cells. Without it, glucose accumulates in the bloodstream, leading to the hallmark symptoms of diabetes, including hyperglycemia and its associated complications.

This discovery was a turning point in medical science. Before Minkowski's work, diabetes was poorly understood, often attributed to kidney malfunction rather than metabolic dysfunction. His findings redirected research towards the endocrine function of the pancreas, laying the groundwork for the eventual isolation of insulin. By the 1920s, insulin became a therapeutic breakthrough, offering the first effective treatment for diabetes. This development saved countless lives and transformed diabetes from a fatal illness into a manageable condition.

Today, Minkowski's work continues to underpin advancements in diabetes care. Modern treatments, including synthetic insulin analogs, continuous glucose monitoring systems, and islet cell transplantation, are direct descendants of his discovery. Furthermore, research into the pancreas' broader role in metabolic diseases, such as type 2 diabetes and pancreatitis, underscores the lasting impact of his hypothesis.

Minkowski’s contributions not only revolutionized diabetes management but also shaped the field of endocrinology, emphasizing the pancreas as a vital organ in maintaining metabolic homeostasis. His work remains a cornerstone of medical science, inspiring ongoing innovation in the quest to improve the lives of individuals with diabetes worldwide.
Oskar Minkowski and the Discovery of the Pancreas’ Role in Diabetes

Insulin level in human body

75% of body cholesterol is produce by liver, which is influence by insulin levels. If the insulin level is optimized, it also will regulate cholesterol level.

Foods that increase insulin levels will also contribute to high cholesterol by making liver produce more of it.

Elevated levels of glucose and insulin are implicated in much age-related disease such as hypertension, heart disease and stroke and are a hallmark of mammalian aging.

The reduction on the levels of glucose and insulin and the lack of glucose byproducts may retard aging in other ways. Glucose byproducts induce cells in the pancreas to secrete insulin after eating.

Most type 2 diabetics are overweight or obese. This is because their fat cells are constantly maintained in fat storage mode by high levels of insulin secreted from the pancreas.

Vitamin E reduces insulin resistance, and that is important because high levels of insulin drain vitamin E from the boy, leaving it at increase risk for heart disease and other injury from free radicals.
Insulin level in human body

Pancreas: organ and its functions

The pancreas is an organ located in the abdomen. The pancreas is positioned beneath and behind the stomach in a location referred to as the retroperitoneum. It is surrounded by the stomach, small intestine, spleen, and liver. It plays an essential role in converting the food into fuel for the body's cells. Pancreas can be thought of as “2 organs in 1”:

Exocrine portion 
•The exocrine function is devoted to secretion of digestive enzymes (such as amylase and lipase), ions and water into the intestine of the gastrointestinal (GI)tract. The digestive enzymes are necessary for converting a meal into molecules that can be absorbed across the surface lining of the GI tract into the body.
•Composed of acinar cells and ducts
•Comprises 80‐90% of the pancreas

Endocrine portion 
•Secretes hormones such as insulin and glucagon
•Composed of Islets of Langerhans

The regions of the pancreas are the head, body, tail and uncinate process. The pancreas is connected by the nervous system containing both sensory neurons and effector neurons. The sensory neurons function for pain perception so that diseases of the pancreas cause significant pain while the effect or neurons are involved in regulating the secretions of both the exocrine and endocrine pancreas.
Pancreas: organ and its functions

β-cells in pancreas

The islets of langerhans consist of insulin-releasing β-cells (65-90%) forming the core of the islet, glucagon-releasing alpha-cells (15-20%), somatostatin-producing delta-cells (3-10%), and pancreatic polypeptide-producing PP-cells (1%) are usually located on the surface.

Increased blood glucose after a meal is countered by the subsequent increased release of the hypoglycemic hormone insulin from the pancreatic β-cells.

The insulin gene is composed of four exons and two introns. the hormone’s precursor (preproinsulin), with 1150 Da, carries a signal peptide that directs the peptide chain to the interior of the endoplasmic reticulum (eR) and contains four peptides: N-terminal signal peptide, B chain, C peptide and A chain.

Insulin is secreted by the endocrine pancreatic β-cells upon an increase in blood glucose to lower the blood glucose level.

Glucose is the principal physiological insulin secretagogue and a potent regulator of β-cells activity. The increased blood glucose, usually occurring after a meal (postprandial), is sensed by the β-cells and glucose is taken up by glucose transporters.

Once inside, glucose is first converted to glucose-6-phosphate by glucokinase and then in the glycolysis to pyruvate, which enters the mitochondria.

Zinc plays an essential role in the regulation of pancreatic β-cells function, affecting important processes including pro-insulin biosynthesis, glucose-stimulated insulin secretion, and cell viability. Mutations in zinc efflux transport protein ZnT8 have been linked with both type 1 and type 2 diabetes.

Type 1 diabetes results from pancreatic β-cells degeneration and is characterized by lack of insulin production, while patients with Type 2 diabetes show a state of insulin resistance and usually relative insulin deficiency.
β-cells in pancreas