polyphagia glycosuria polyuria and polydipsia let's go through them one by one even though there's a lot of glucose

in the blood it can't get into the cells

which leaves cells start for energy so in response to adipose tissue starts breaking down fat called lipolysis and muscle tissue starts breaking down
proteins both of which results in weight loss for someonewith uncontrolled diabetes thiscatabolic state leaves people feelinghungry also known as poly
Fei Jie FeiJie means eating and poly means a lotnow with high glucose levels that meansthat when blood gets filtered throughthe kidneys some of it
starts to spillinto the urine called glycosuria glycostore first to glucose and urea or firstto the urinesince glucose is osmotically activewater tends to follow
it resulting in anincrease in urination or polyuria polyagain refers to a lot in urea againrefers to urine finally because there'sso much urination people
withuncontrolled diabetes become dehydratedin thirsty or polydipsia poly means alot and Dipsy amines thirst even thoughpeople with diabetes aren't
able toproduce their own insulin they can stillrespond to insulin so treatment involveslifelong insulin therapy to regulatetheir blood glucose levels and
basically enable their cells to use glucose

Now, let’s switch gears and talk about Type 2 diabetes, which is where the body makes

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insulin, but the tissues don’t respond as well to it.

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The exact reason why cells don’t “respond” isn’t fully understood, essentially the

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body’s providing the normal amount of insulin, but the cells don’t move their glucose transporters

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to their membrane in response, which remember is needed for glucose to get into the cell,

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these cells therefore they have insulin resistance.

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Some risk factors for insulin resistance are obesity, lack of exercise, and hypertension,

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and the exact mechanisms are still being explored.

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For example, an excess of adipose tissue—or fat—is thought to cause the release of free

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fatty acids and so-called “adipokines”, which are signaling molecules that can cause

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inflammation, which seems related to insulin resistance.

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However, many people that are obese are not diabetic, so genetic factors probably play

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a major role as well.

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We see this when we look at twin studies as well, where having a twin with type 2 diabetes

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increases the risk of developing type 2 diabetes, completely independent of other environmental
10:04

risk factors.

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In Type 2 diabetes, since tissues don’t respond as well to normal levels of insulin,

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the body ends up producing more insulin in order to get the same effect and move glucose

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out of the blood.

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They do this through beta cell hyperplasia, an increased number of beta cells, and beta

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cell hypertrophy, where they actually grow in size, all in this attempt to to pump out

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more insulin.

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This works for a while, and by keeping insulin levels higher than normal, blood glucose levels

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can be kept normal, called normoglycemia.

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Now, along with insulin, beta cells also secrete islet amyloid polypeptide, or amylin, so while

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beta cells are cranking out insulin they also secrete an increased amount of amylin.

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Over time, amylin builds up and aggregates in the islets.

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This beta cell compensation, though, isn’t sustainable, and over time those maxed out

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beta cells get exhausted, and they become dysfunctional, and undergo hypotrophy and

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get smaller, as well as hypoplasia and die off.

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As beta cells are lost and insulin levels decrease, glucose levels in the blood start

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to increase, and patients develop hyperglycemia, which leads to similar clinical signs that

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I mentioned before, like polyphagia, glycosuria, polyuria, and polydipsia.

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But unlike type 1 diabetes, there is generally some circulating insulin in type 2 diabetes
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from the beta cells that are trying to compensate for the insulin resistance.

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This means that the insulin/glucagon balance is such that diabetic ketoacidosis doesn’t

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usually develop.

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Having said that, a complication called hyperosmolar hyperglycemic state (or HHS) is much more

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common in type 2 diabetes than type 1 diabetes - and it causes increased plasma osmolarity

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due to extreme dehydration and concentration of the blood.

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To help understand this, remember that glucose is a polar molecule that cannot passively

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diffuse across cell membranes, which means that it acts as a solute.

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So when levels of glucose are super high in the blood (meaning it’s a hyperosmolar state),

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water begins to leave the body’s cells and enter the blood vessels, leaving the cells

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relatively dry and shriveled rather than plump and juicy.

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Blood vessels that are full of water lead to increased urination and total body dehydration.