Tuesday, January 13, 2009

BMI vs. Waist circumference

Despres J, Lemieux I, Bergeron J, et al. Abdominal Obesity and the Metabolic Syndrome: Contribution to Global Cardiometabolic Risk. Arterioscler Thromb Vasc Biol. 2008;28(6):1039-1049.

This is a great review article about the issue of abdominal and more importantly visceral fat and its relationship to metabolic complications.
It is too difficult to summarize the review article since there are just too many great points and supporting studies listed, so I just wanted to give a brief glimpse into the paper.
One of the points made in the article is the proposed mechanisms for visceral tissue and its relationship/cause of insulin resistance:
  • The hyperlipolytic state of the omental adipose tissue, which shows resistance to the action of insulin, contributes to expose (through the portal circulation) the liver to high concentrations of free fatty acids, impairing several hepatic metabolic processes leading to hyperinsulinemia (decreased insulin clearance), glucose intolerance (increased hepatic glucose production), and hypertriglyceridemia (increased VLDL-apolipoprotein B secretion).
  • The adipose tissue is a remarkable endocrine organ which is a source of adipokines like adiponectin and inflammatory cytokines such as interleukin (IL)-6 (IL-6) and tumor necrosis factor (TNF)-{alpha} (to only name a few) which contribute to the insulin resistant, proinflammatory, -thrombotic, and -hypertensive state of visceral obesity.
  • Excess visceral adiposity is only (or partly) a marker of the relative inability of subcutaneous adipose tissue to act as a protective metabolic sink because of its inability to expand (lipodystrophy) or because it has become hypertrophied, dysfunctional and insulin resistant. Under this third scenario, sedentary individuals who cannot store their energy surplus in the subcutaneous adipose tissue would be characterized by accumulation of fat at undesired sites such as the liver, the heart, the skeletal muscle, and the pancreas. They list a study that showed men with a great deal of visceral fat remained hyper-triglyceridemic 8 hours after an oral fat load.
I thought that this last point of the inability to store energy properly was a great mechanism.
Another point the authors raise is whether we should measure loss of waist circumference instead of weight with the initiation of exercise regimen since people can gain muscle and lose fat resulting in no net weight loss.


  1. This is very interesting.
    Can a person change from one phenotype of adipose depositition to another during their lifetime. In otherwords, is there an upstream trigger for the deposition pattern of visceral fat?

    Great post. Very thought provoking.

  2. That is a great point and unfortunately we don't know all the answers. Are people born with a predisposition to store fat viscerally (possibly due to inability to handle energy storage well) or is it due to the accumulation of a certain amount of fat stores. Also because of the difference between men and women in this regard, could there be a hormonal etiology?

  3. That's very interesting. I was wondering have they done any studies that you know of regarding people (or animals) status post omentectomy? It seems like it would be of benefit in light of bullet #1, but maybe not in light of #3.


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