LPL and Weight Gain: How the Chemistry of Lipoprotein Lipase Further Eviscerates the Idea That "Calories Count"

LPL -- also known as lipoprotein lipase -- is an enzyme that seems to be critical in terms of how and where the body distributes fat tissue. As science writer Gary Taubes details on pages 397 to 399 of Good Calories Bad Calories, the actions of this enzyme explain many of the underlying mysteries about why we accumulate fat where we do -- for instance, why we get beer bellies and fat thighs as opposed to fat foreheads and plump palms.

That this hormone appears to play a crucial role in fat regulation has huge implications for our two hypotheses about what causes obesity. As Taubes explains elsewhere in Good Calories Bad Calories, most people assume that the 1st law of thermodynamics requires that "calories count" because weight gain associates with the establishment of a positive caloric balance. Hence we have the Caloric Balance Hypothesis. But this theory gives us no explanation whatsoever for why and how and where we get fat.

The other theory -- the Lipophilia Hypothesis -- tells us that hormones and enzymes and other physiological factors control fat deposition and mobilization.

In other words, if LPL does play a key role in fat tissue regulation, it's a huge problem for Caloric Balance and a boost for Lipophilia.

So, what does the evidence tell us?

1. Taubes argues that insulin and other hormones orchestrate LPL activity. This explains why certain areas of the body are more likely than others to get fat. It also explains why fat distribution is different based on whether you are a man or a woman, and it explains why our fat distribution changes as we get older or (if you are a woman) go through menarche and menopause.[1]

2. Here's another article that seems to confirm this crucial role of lipoprotein lipase: "Lipoprotein lipase: a multifunctional enzyme relevant to common metabolic diseases."[2]

3. And here is another paper: "Tissue specific overexpression of lipoprotein lipase causes tissue specific insulin resistance."[3]

From the title alone, this seems to imply that LPL has a serious and significant role in the metabolic process, just as Taubes alleges.

4. Here's another article: "Alterations in lipoprotein lipase in insulin resistance."[4]

5. And here's yet another article: "Relation between insulin resistance, hyperinsulinemia, post heparin plasma lipoprotein lipase activity, and postprandial lipemia."[5]

These papers don't argue directly for Lipophilia. But by confirming that LPL plays a big role in regulating fat metabolism, they support the notion that calories don't actually "count" and thus lend more credibility and coherence to the Lipophilia Hypothesis.

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Return to main page on the debate about what roles LPL and fat tissue play in metabolism


References


1. Taubes, Gary. "Good Calories, Bad Calories." p 398. New York: Knopf (2007).

2. RH Eckel. "Lipoprotein lipase: a multifunctional enzyme relevant to common metabolic diseases." NEM Volume 320:1060-1068 April 20, 1989 Number 16.

3. Kim JK, Fillmore JJ, Chen Y, Yu C, Moore IK, Pypaert M, Lutz EP, Kako Y, Velez-Carrasco W, Goldberg IJ, Breslow JL, Shulman GI. "Tissue specific overexpression of lipoprotein lipase causes tissue specific insulin resistance." Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7522-7. Epub 2001 Jun 5.

4. Eckel RH, Yost TJ, Jensen DR. "Alterations in lipoprotein lipase in insulin resistance." Int J Obes Relat Metab Disord. 1995 May;19 Suppl 1:S16-21.

5. Jorgen Jeppesen; Clarie B. Hollenbeck; M.-Y. Zhou; Ann M. Coulston; Claire Jones; Y.-D. Ida Chen; Gerald M. Reaven. "Relation between insulin resistance, hyperinsulinemia, post heparin plasma lipoprotein lipase activity, and postprandial lipemia." (Arteriosclerosis, Thrombosis, and Vascular Biology. 1995;15:320-324.)© 1995 American Heart Association, Inc.

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