Diabetes mellitus occurs due to deficiency of insulin function which may occur due to
1. decreased insulin release or
2. insulin resistance.
In diabetes, storage and utilisation of glucose decreases in fed state leading to increase in blood glucose concentration after food i.epost-prandial hyperglycemia. Due to continuing glycogenolysis and gluconeogenesis, glucose concentration in blood rises in between meals too i. e fasting hyperglycemia
Due to excess blood glucose concentration, the glucose filtered through nephron is also high. This exceeds the capacity of nephrons of absorbing glucose i.e transport maximum is reached, above which the nephrons are not able to reabsorb further glucose and hence glucose starts appearing in urine i.e glucosuria occurs. The presence of glucose in nephron acts as anosmotic pull for water preventing the reabsorption of water also from the nephron. So water loss also increases causing increase in the volume of urine i.e polyuria. Due to increase in water loss from the body, and hyperosmolarity of blood due to increased blood glucose concentration, water moves out of cells. This when happens in osmoreceptors…thirst centres are activated causing increase in the intake of water i.e polydipsia.
Hyperphagia: When insulin is deficient, the satiety centre neurons are not able to utilise glucose and become inactive. Thus they do not inhibit feeding centre. Since feeding centre is not inhibited, the person feels hungry and eats often i.e polyphagia occurs.
In insulin deficiency lipolysis starts in adipose tissue causingrelease of free fatty acids in circulation, proteolysis also starts. So with increased lipolysis and proteolysis , there is weight loss. The free fatty acids enter liver and undergo beta oxidation leading ultimately to formation of acetyl COA. In diabetes, most of the acetyl coA is channeled away from Krebs cycle and is utilised for production of ketone bodies (ketosis). When rate of productions of ketone bodies is too high which occurs when insulin levels are very low or virtually absent as seen in type 1 diabetes mellitus, ketone bodies decrease blood pH (ketocacidosis) .
Since blood pH decreases, body starts compensatory mechanisms for excretion of excess acids by increasing respiratory rate and depth. This is known as Kussmaul’s breathing or air hunger, Some ketone bodies i.e acetone is also excreted by breath causing fruity smell of breath. Ketoacidosis is always accompanied by dehydration. This leads to activation of renin-angiotension-aldosterone system. Thus causing hyperaldsteronism causing potassium loss from the body.
In type 2 DM, ketocacidosis is not that common, since insulin receptor defect starts slowly, i.e some actions of insulin are preserved so lipolysis and proteolysis are not that severe. Since lipolysis is not severe, formation of ketone bodies is also not excessive. In contrast, another problem may occur in type 2 diabetes i.e hyperglycemia hyperosmolar state. In this also, there is hyperglycemia, causing high serum osmolarity , also causing glucosuria and poyluria and hence depletion of watre. However, ketoacidosis is not present.
Functionsof insulin: https://youtu.be/JjUaj6v2vqI
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