Blood glucose control and diabetes overview
Homeostasis and response • Hormonal coordination in humans
Flashcards
Test your knowledge with interactive flashcards
Key concepts
What you'll likely be quizzed about
Insulin: action and effect
Insulin is a hormone produced by beta cells in the pancreas when blood glucose rises after a meal. Insulin increases uptake and use of glucose by target cells and stimulates the conversion of glucose into glycogen in the liver and muscles, thereby lowering blood glucose concentration. Insulin binding at cell membranes increases glucose transport into cells and activates enzymes that synthesise glycogen. Increased cellular uptake and storage cause a fall in blood glucose that eventually reduces insulin secretion via negative feedback.
Glucagon and negative feedback (higher tier)
Glucagon is a hormone produced by alpha cells in the pancreas when blood glucose falls. Glucagon stimulates the liver and muscle cells to break down glycogen into glucose and to release glucose into the blood, raising blood glucose concentration. Insulin and glucagon act in opposition within a negative feedback cycle: a rise in blood glucose increases insulin release and decreases glucagon release; a fall in blood glucose increases glucagon release and decreases insulin release. This continuous opposing action maintains blood glucose within a narrow range.
Glycogen formation and storage
Glycogen is an insoluble polymer of glucose stored mainly in liver and muscle cells. Excess blood glucose converts into glycogen by enzyme-controlled reactions in the liver and muscle, reducing the concentration of glucose in blood. When blood glucose falls, enzymes break glycogen down back into glucose for release into the blood. Glycogen storage provides a rapid source of glucose for short-term energy and assists homeostatic regulation.
Type 1 diabetes: cause and features
Type 1 diabetes results from destruction of insulin-producing beta cells in the pancreas, commonly through an autoimmune reaction, which prevents sufficient insulin production. Blood glucose rises rapidly after food intake because the pancreas cannot secrete insulin to stimulate glucose uptake or glycogen formation. Symptoms commonly include high blood glucose, thirst, frequent urination and tiredness. Management requires replacing the missing insulin and lifestyle measures to control peak glucose levels.
Type 2 diabetes: cause and features
Type 2 diabetes usually arises later in life and involves reduced sensitivity of liver and muscle cells to insulin or insufficient insulin production. Cells fail to respond to normal insulin levels, so conversion of glucose to glycogen decreases and blood glucose remains elevated. Risk factors include sedentary lifestyle, unhealthy diet and obesity. Symptoms develop more slowly than in Type 1 and become apparent as sustained hyperglycaemia causes systemic effects.
Treatments for Type 1 and Type 2
Type 1 diabetes treatment replaces insulin by injections or continuous infusion pumps to control post‑meal glucose rises; diet and regular exercise reduce insulin requirements. Insulin from genetically modified bacteria provides human insulin for injections. Type 2 treatment focuses on diet modification, increased exercise, weight loss and medications that improve insulin sensitivity or increase insulin secretion; insulin injections are less common because many cells do not respond to injected insulin. Preventing obesity reduces population risk.
Interpreting blood glucose graphs
Graphs of blood glucose vs time after a meal show a rapid rise then a fall in healthy responses as insulin acts to store glucose as glycogen. In Type 1 diabetes, graphs show higher peaks and slower return to baseline without injected insulin. In Type 2 diabetes, graphs show elevated levels with a blunted fall because of reduced cellular response. Key graph skills include reading peak glucose values, time to return toward baseline, comparing two patients on the same axes, and linking differences to insulin secretion or cellular response. Data extraction from tables and plotting supports these interpretations.
Obesity and diabetes: evaluation
Obesity increases the risk of developing Type 2 diabetes by promoting insulin resistance in liver and muscle cells. Excess adipose tissue and associated metabolic changes reduce cellular responsiveness to insulin, so blood glucose regulation becomes less effective. Population increases in obesity correlate with rising Type 2 prevalence. Causal strength varies between individuals; genetics, age and activity level modify risk. Weight loss and increased exercise reduce risk and improve glucose control, demonstrating a modifiable relationship between obesity and Type 2 diabetes.
Key notes
Important points to keep in mind