Nutritional Endocrinology Practitioner Training (NEPT)
Clinical Pearl

December 10th, 2017

The continuing saga of  insulin resistance and fat

I’m continuing to review the studies I shared with you a couple of weeks ago,  with the intention for writing a comprehensive blog post in January. This week, I chose to analyze this article:

Lipid overload and overflow: metabolic trauma and the metabolic syndrome

https://www.ncbi.nlm.nih.gov/pubmed/14580758 – this is the abstract.  I purchased the full study, and it’s HERE but don’t post this or publish it anywhere as it’s just for NEPT members.

http://drritamarie.s3.amazonaws.com/materials/INE/LipidOverloadAndOverflow-Insulin-Resistance-Metabolic-Syndrome.pdf

This article takes an interesting perspective on the etiology of insulin resistance, and it’s relationship to lipogenesis.  

The author does not address dietary fat as a cause of insulin resistance; rather he addresses “overnutrition” and “underexertion” He makes 3 very good points:

1. Insulin resistance of obesity triggers insulin-stimulated lipogenesis  – meaning that resistance to insulin uptake of glucose triggers the creation of fat.
2. Resistance to the  uptake of surplus glucose might be a defense against lipid overaccumulation in lean tissues
3. The underlying cause of the metabolic syndrome is leptin-resistance.

 

According to this article, insulin induces expression of the enzymes of lipogenesis through upregulation of the lipogenic transcription factor, SREBP-1c.

He observes that when obesity is induced in normal rats by overfeeding, a diet of 60% fat, most of the excess fat (96%) is deposited in adipose tissue.  In leptin resistant rats, even on a low fat diet, much of the excess is deposited in non-adipose tissue.

So what is the true cause of insulin resistance?  It would appear to related to consuming more calories that are burned.  Nothing in this article differentiates between fat calories and sugar calories.