type 2 diabetes native americans

insulin

blood sugar regulating hormone produced by the pancreas

beta cells

insulin producing cells

cytokines

proteins that help cells communicate

insulin resistance

when the body dosent normally respond to insulin

FFAs

unbound fatty acid moleculues

hyperglycemia

high blood sugar

atheroclerosis

fatty plaque acid build up in arteries

endothelial injury

damage to inside of blood vessels

neuropathy

damage to blood vessels in kidneys, leads to imparied function

retinopathy

damange to blood vessels in the eye leads to impaired function

glucagon

hormone produced by the pancreas that raises blood sugar

chemical level patho

high blood glucose levels and fatty acids

Reduced glucose uptake

inflammatory molecules block insulin signaling

beta cell stress begins

insulin responsive cells

become resistant

beta cells try to make insulin but

become less responsive and exhibit dysfunction this becomes worse over time

macrophages begin producing certain

cytokines that encourage insulin resistance as well as metabolic dysfunction

pancreas

beta cell dysfunction due to overworking and excess fatty acids

glucotoxicity damages cells which reduce insulin secretion

beta cell mass decreases due to inflammation and stress

pancreatic insulin production drops

liver

liver produces glucose despite high insulin levels

muscles

poor glucose uptake

adipose tissue

enlarged fat cells release FFAs

endocrine/metabolic

bodywide insulin resistance, decreased insulin production, hyperglycemia, lipid metabolism dysfunction

cardiovascular

accelerated atherosclerosis, endothelial injuries, and higher risk for hyper tension

urinary system

nephropathy

nervous

chronic glucotoxicity damages peripheral and autonomic nerves

the combined system dysfunction leads to disease

Symptoms emerge, complications accumulate: cardiovascular disease, neuropathy, nephropathy, retinopathy

symptoms

polyuria (frequent urination), unintended weight loss, polydipsia (excessive thirst), blurred vision, fatigue, itchiness

risk fators

family history

genetic predisposition

older age

obesity

sedentary lifestyle

unhealthy diet (high sugar, cals and carbs)

fatty lver

high BP

prediaetic

metabolic syndrome

treatments medication

Biguandines

SGLT2 inhibits

GLP 1 receptor agonists

DPP 4 inhibitors

Sulfonylueras

Thiazolidinediones (TZD)

interventions and therapies

insulin therapy, dietary changes, exercise, weight management

future therapies

TRIPLE agonist medications combines GLP 1, GLP and glucagon inhibitors

Beta cell regeneration & preservation

gene therapy

improved insulin delivery

artificial pancreas systems

early stage disease

insulin resistance beings

muscle liver and fat tissue stop responding normally to insulin

pancreas tries to compensate

often associated with obesity inactivity or genetics

intermediate stage of disease

beta cells start to fatigue

prediabetes begins

still reversible

diagnosis

beta cells unable to keep up leads to hyperglycemia

symptoms persist

treatment begins

long term progression

complications being

CV disease, neuropathy, nephropathy, retinopathy