Which comes first – obesity or Hyperinsulinemia? Does fat get locked in our cells due to higher fasting insulin levels? Or is it the fact that we are fat that raises our fasting insulin levels?
From (Crofts, C., Zinn, C., Wheldon, M., Schofield, G. 2015. Hyperinsulinemia: A unifying theory of chronic disease?. Diabesity 1(4): 34-43.):
It is agreed that hyperinsulinemia precedes hyperglycemia, by up to 24 years. There is a strong argument that hyperglycemia indicates pancreatic β-cell attrition; essentially end-stage organ damage.We contend that the under-recognition of hyperinsulinemia is an important clinical issue because there are no standard diagnostic reference values, is most accurately diagnosed with dynamic glucose and insulin testing, and has few (pharmaceutical) management options.
One of the posited reasons for hyperinsulinemia is fructose.
Fructose is metabolized in liver into ATP and/or triglycerides in a process that is competitive with, and preferential to, glucose. If excessive fructose is consumed, glucose will not be metabolized causing hyperglycemia and subsequent hyperinsulinemia.
A helpful insight:
Hyperinsulinemia is independent to insulin resistance: Hyperinsulinemia is excessive insulin secretion, while insulin resistance is impaired glucose uptake.
Given the intertwined nature between insulin resistance and hyperinsulinemia as depicted above, it can be assumed that the majority of people with insulin resistance are also hyperinsulinemic.
Here’s another subject that is interesting:
There is debate as to whether hyperinsulinemia precedes, or are a consequence of fatty liver
From the citation noted (Dig Liver Dis. 2010 May;42(5):320-30. From the metabolic syndrome to NAFLD or vice versa? Vanni E, et.al.):
Recent data indicate that hyperinsulinemia is probably the consequence rather than cause of NAFLD and NAFLD can be considered an independent predictor of cardiovascular disease. Serum free fatty acids derived from lipolysis of visceral adipose tissue are the main source of hepatic triglycerides in NAFLD, although hepatic de novo lipogenesis and dietary fat supply contribute to the pathogenesis of NAFLD.
Here’s more on the fat question:
Hypertrophic adipose tissues activate inflammatory and stress pathways and decreases insulin response. This results in increased cytokine production including TNF-α, vascular endothelial growth factor and leptin, while adiponectin expression is decreased. These actions contribute to decreased glucose and lipid uptake, leading to further reductions to adiponectin secretion and adipogenesis as well as contributing to further insulin resistance. Decreased glucose uptake means there is less glycerol within the adipocyte to esterify free fatty acids, allowing them to infiltrate and accumulate in other tissues.
Sounds like a viscous cycle!