A recent study identifies the mechanism of pancreatic cells secreting high insulin levels eventually leading to explain how type 2 diabetes develops in humans. The reason behind the over secretion of insulin by the pancreatic cells; beta cells is the central question in diabetes research. The general theory was that maybe the body is in the process of being deaf to insulin in result the beta cells start secreting more insulin to compensate. But isolated beta cells still over-secreting insulin which shows the gap in that theory.
The study was published in a journal: American Diabetes Association’s journal Diabetes.
Beta cells are found in the pancreatic islets and their primary function is to synthesize and release insulin and amylin hormone. Both reduced blood glucose levels by several mechanisms. Insulin release is stimulated by the presence of blood glucose levels.
Type 2 diabetes is non-insulin dependent diabetes, also known as chronic hyperglycemia. Its main causes are the development of metabolic syndromes or genetics. Here body develops resistance against insulin and shows a declined response but beta cells are still secreting the glucose. But because of the declined response beta cells become exhausted by the overstimulation. There is not enough insulin production for keeping the blood glucose level in the normal range.
In the recent study, scientists are setting goals to understanding another mechanism other than insulin resistance and increased glucose levels which might help how diabetes develops. The researchers found a pathway that is glucose independent and sensitive to fatty acids drives insulin secretion in the initial stages of diabetes.
The study covers the details about physiology and pathophysiology of type 2 diabetes mellitus including different aspects of laboratory, human and animal research.
According to an estimation of the World Health Organization (WHO), one in eleven people suffer from diabetes and it was the cause of 1.62 million deaths in 2016 based on the latest available data. Diabetes is designated as one of four major noncommunicable diseases.
One of the professors of endocrinology and pharmacology at the David Geffen School of Medicine at UCLA and senior author of the study, Orian Shirihai used pre-diabetic mice for studying the mechanisms of insulin secretion in the glucose absence.
The researchers found that the protein in beta cells of prediabetic and obese animals, known as Cyclophilin D induced a proton leak phenomenon. This proton leak promoted the secretion of insulin in the absence of increased glucose. This mechanism was dependent on the fatty acids, normally incapable of the stimulation of insulin secretion in healthy animals.
Obese mice lacking CypD gene didn’t secrete excess levels of insulin. The researchers confirmed that the same process was happening in the isolated human pancreatic cells; in the presence of fatty acids on levels that will be common in obese people, the cells exhibited insulin secretion in the absence of the increased level of glucose.
The outcomes suggest the new methods for the prevention of the insulin resistance and the treatment of diabetes and to halt its progression by blocking the proton leak mechanism n the beta cells.