Diabetes Physiology Study Notes

A condition where fasting blood sugar levels are slightly elevated but not high enough to be classified as type 2 diabetes. This indicates an early stage of insulin resistance, where the body is not effectively using insulin to lower blood sugar.

A condition where blood sugar levels are elevated after a sugar-loaded drink, but not high enough to be classified as type 2 diabetes. This signifies reduced insulin sensitivity, where the body struggles to process sugar efficiently.

The primary factor causing type 2 diabetes, accounting for 80-85% of the risk. It is characterized by an imbalance between energy intake and expenditure, leading to excessive body weight.

This refers to the genetic predisposition to developing type 2 diabetes. While no single gene is responsible, multiple genes contribute to a person's susceptibility to the disease.

This refers to the process of reducing energy intake and increasing energy expenditure, ultimately leading to weight loss. It is a key factor in preventing and managing type 2 diabetes.

A metabolic pathway that converts fructose-6-phosphate into UDP-N-acetylglucosamine (UDP-GlcNAc).

The enzyme that catalyzes the first step of the HBP, converting fructose-6-phosphate to glucosamine-6-phosphate.

A sugar molecule attached to proteins through a specific process called O-GlcNAcylation.

The process of attaching UDP-GlcNAc to serine and threonine residues on proteins, modifying their function.

A crucial protein involved in insulin signaling, responsible for glucose uptake in cells.

A condition of high blood glucose levels, which can increase the flux through the HBP, leading to increased O-GlcNAcylation.

The state of reduced responsiveness to insulin, often caused by excessive O-GlcNAcylation.

The process of increasing the pancreatic β-cell mass and insulin production to compensate for insulin resistance.

An artificial pancreas system that combines a continuous glucose monitor (CGM) and an insulin pump, providing automated insulin delivery based on real-time glucose levels.

A treatment option for type 1 diabetes involving transplanting healthy pancreatic islet cells, responsible for insulin production. This can lead to insulin independence for a significant period but may require multiple transplants due to beta cell decline.

Refers to the ability of the body to utilize insulin properly, allowing glucose to enter cells for energy.

Refers to the ability of the pancreas to produce sufficient insulin, the hormone responsible for regulating blood glucose.

Individuals who have been identified as having a genetic risk for developing type 1 diabetes but have not yet developed autoantibodies.

Those with multiple autoantibodies indicating predisposition to type 1 diabetes but without hyperglycemia.

The process by which the body's immune system mistakenly attacks and destroys insulin-producing beta cells in the pancreas, leading to type 1 diabetes.

The stage of type 1 diabetes where the body struggles to maintain normal glucose levels due to reduced insulin production.

A type of insulin therapy that is typically the first line of treatment for type 2 diabetes when oral medications and combination therapies don't work.

A lifestyle change that significantly reduces the risk of developing type 2 diabetes.

A dietary approach that emphasizes fruits, vegetables, legumes, olive oil, and fish, while limiting meat and dairy products.

A compound found in red grapes and red wine with potential insulin-sensitizing effects.

A type of enzyme that plays a role in cellular energy homeostasis and is activated by Resveratrol.

The process of increasing insulin sensitivity, which allows the body to use insulin more effectively.

The control of blood pressure, which is a key aspect of reducing the risk of cardiovascular disease.

The control of blood glucose levels, which plays a crucial role in managing diabetes and reducing the risk of heart disease.

A class of medications that lowers blood glucose levels by blocking the reabsorption of glucose and sodium back into the bloodstream through the kidneys.

SGLT2 inhibitors block the sodium-glucose co-transporter 2 (SGLT2) protein in the proximal tubules of the kidneys.

By blocking glucose reabsorption, SGLT2 inhibitors increase the excretion of glucose in the urine.

Lower blood glucose levels, weight loss due to calorie loss in urine, reduced blood pressure, lower uric acid levels, and improved cardiovascular & renal outcomes.

Renal impairment, liver disease, heart failure, severe infection, dehydration, metabolic acidosis.

Personal or family history of medullary thyroid carcinoma, multiple endocrine neoplasia syndrome type 2.

SGLT2 inhibitors have a lower risk of causing hypoglycemia compared to some other diabetes medications because their action depends on the presence of glucose.

Metformin (Biguanides), GLP-1 Analogues.

AMPK promotes the breakdown of stored fat (triglycerides) to provide energy for the body by regulating the entry of fatty acids into mitochondria where they can be burned for energy. This process involves inhibiting an enzyme called ACC (Acetyl-CoA carboxylase) which decreases the production of Malonyl-CoA, a molecule that prevents fatty acid entry into the mitochondria.

Insulin resistance is a condition where the body's cells become less responsive to insulin, a hormone that helps regulate blood sugar. This leads to increased glucose production in the liver (gluconeogenesis) and decreased glucose uptake by muscles and other tissues, resulting in higher blood sugar levels.

The diacylglycerol pathway is involved in glycogen synthesis, a process that stores glucose as a complex carbohydrate for later use. This pathway includes key enzymes like PI3K, Akt2, and GSK3β, which play a role in regulating glycogen synthesis.

Triglycerides are a type of fat stored in fat cells (adipocytes). When broken down, they release Free Fatty Acids (FFAs) and glycerol. Glycerol is used by the liver to produce glucose through a process called gluconeogenesis.

Insulin resistance leads to decreased PI3K activity in the liver and muscles, which impairs glucose uptake. This reduced uptake leads to increased glucose production in the liver (gluconeogenesis).

The transcription factor FOXO-1 is activated in insulin resistance, leading to increased production of enzymes involved in gluconeogenesis. This results in higher glucose production in the liver even when blood sugar is high.

Insulin resistance also decreases glycogen synthesis due to reduced phosphorylation of GSK3β, an enzyme crucial for glycogen synthesis. This means the body stores less glucose as glycogen, contributing to higher blood sugar levels.

The Glycaemic Index (GI) of a food reflects how quickly it raises blood sugar levels after consumption. Foods with a high GI cause a rapid spike in blood sugar, whereas low GI foods lead to a slower and more sustained rise. This effect is particularly relevant for individuals with type 2 diabetes, as maintaining stable blood sugar levels is crucial for managing the disease.