mcts etc.

[Guest guest]

At 10:27 AM 8/19/2006, you wrote:

>1: Nutr Hosp. 2006 Jul-Aug;21(4):552-5. Links

>[Eucaloric substitution of medium chain triglycerides for dietary long

>chain fatty acids improves body composition and lipid profile in a patient

>with human immunodeficiency virus lipodystrophy]

Interesting...but what the hell does it mean?

Well, practically speaking, it can mean things like FISH OIL (see, e.g.,

Medicine. 82(2):129-146, March 2003, where they note " Severe

hypertriglyceridemia should be treated with a very low-fat diet and

[omega]-3 polyunsaturated fatty acid supplementation from fish oils. "

Coconut oil (or lauric acid) is another possibly (and another " cure de

jour " I know--but what the hell...it tastes good to some folks!)

That is to say, a fatty acid is made up of a string of carbon atoms. If you

have 18-20, that's considered a long chain. The kind found in vegetable

oils such as corn oil, safflower oil, peanut oil or cottonseed oil. So

these are the kind of fats you want to reduce in your diet. Sadly, they're

also ubiquitous...unless you can manage to avoid processed or prepared/fast

food. Screw Fritos. Screw Coke (OK, that's the carbohydrate issue of high

fructose death syrup).

A triglyceride is a set of 3 fatty acids attached to a glycerol backbone.

The structure of your triglycerides is dependent in part on the supply of

fats you eat. You are what you eat....

See the interesting abstract below from 1983! (When patient health ruled

scientific endeavors and not just profits...oh dear. Broken record

syndrome...surely there's a drug for that! A newly minted disease! Hey,

Glaxo!! BMS!! Somebody PLEASE pass the OxyContin.)

M.

***

http://jcem.endojournals.org/cgi/content/abstract/57/3/517

Journal of Clinical Endocrinology & Metabolism, Vol 57, 517-523, Copyright

© 1983 by Endocrine Society

Eucaloric substitution of medium chain triglycerides for dietary long chain

fatty acids in acquired total lipodystrophy: effects on

hyperlipoproteinemia and endogenous insulin resistance

DE , IF Chan, KB son, SC Horton and C Schipke

Previous studies have suggested that reduction of dietary fat intake, with

or without caloric restriction, may lead to improvement in certain of the

characteristic abnormalities that accompany total lipodystrophy (TLD). We

have studied the effects of eucaloric medium chain triglyceride (MCT)

substitution for dietary long chain fatty acids in a patient with acquired

total lipodystrophy and unusual somatic and visceral anomalies. The patient

exhibited insulin resistance, carbohydrate intolerance, striking fasting-

and glucose-stimulated hyperinsulinemia, hyperglucagonemia, type V

hyperlipoproteinemia, and lipoprotein lipase deficiency on a normal diet.

Improvement in chylomicronemia, hypertriglyceridemia, and xanthomatosis

occurred during eucaloric MCT substitution. Carbohydrate intolerance

decreased and fasting immunoreactive glucagon and insulin concentrations

fell 37% and 83%, respectively. Plasma triglyceride polyunsaturated fatty

acid concentrations decreased to very low levels. With long term MCT

feeding supplemented by polyunsaturated fatty acids, hepatomegaly has

gradually decreased, while body weight has remained stable. The patient has

not yet required insulin therapy. These observations suggest that the

abnormalities in carbohydrate metabolism are closely linked to, and perhaps

dependent on, the abnormalities in lipoprotein transport in TLD. Long chain

triglyceride restriction and MCT supplementation should be attempted in

additional patients with the features of TLD to determine whether this is a

generally effective therapeutic approach.

**

http://www.jbc.org/cgi/content/abstract/276/26/23661

J. Biol. Chem., Vol. 276, Issue 26, 23661-23666, June 29, 2001

Defective Fatty Acid Uptake in the Spontaneously Hypertensive Rat Is a

Primary Determinant of Altered Glucose Metabolism, Hyperinsulinemia, and

Myocardial Hypertrophy*

Tahar Hajri

Dagger

, Azeddine Ibrahimi

Dagger

, T. Coburn

Dagger

, F. F. Knapp Jr.§, Ted Kurtz¶, Pravenec

||

, and Nada A. Abumrad

Dagger

**

From the

Dagger

Department of Physiology and Biophysics, State University of New York at

Stony Brook, Stony Brook, New York 11794-8661, the § Nuclear Medicine

Program, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37831, the ¶

Department of Laboratory Medicine, University of California, San Francisco,

California 94143-0134, and the

||

Institute of Physiology, Czech Academy of Sciences, 14220 Prague, Czech

Republic

Genetic linkage studies implicated deficiency of CD36, a membrane fatty

acid (FA) transporter, in the hypertriglyceridemia and hyperinsulinemia of

the spontaneously hypertensive rat (SHR). In this study we determined

whether loss of CD36 function in FA uptake is a primary determinant of the

SHR phenotype. In vivo, tissue distribution of iodinated, poorly oxidized

beta

-methyliodophenyl pentadecanoic acid (BMIPP) was examined 2 h after its

intravenous injection. Fatty acid transport was also measured in vitro over

20 to 120 s in isolated adipocytes and cardiomyocytes obtained from SHR and

from a congenic line (SHRchr4) that incorporates a piece of chromosome 4

containing wild-type CD36. SHR heart and adipose tissue exhibited defects

in FA uptake and in conversion of diglycerides to triglycerides that are

similar to those observed in the CD36 null mouse. However, a key difference

in SHR tissues is that fatty acid oxidation is much more severely impaired

than fatty acid esterification, which may underlie the 4-5-fold

accumulation of free BMIPP measured in SHR muscle. Studies with isolated

adipocytes and cardiomyocytes directly confirmed both the defect in FA

transport and the fact that it is underestimated by BMIPP. Heart, oxidative

muscle, and adipose tissue in the SHR exhibited a large increase in glucose

uptake measured in vivo using [18F]fluorodeoxyglucose. Supplementation of

the diet with short-chain fatty acids, which do not require

CD36-facilitated transport, eliminated the increase in glucose uptake, the

hyperinsulinemia, and the heart hypertrophy in the SHR. This indicated that

lack of metabolic energy consequent to deficient FA uptake is the primary

defect responsible for these abnormalities. Hypertension was not alleviated

by the supplemented diet suggesting it is unrelated to fuel supply and any

contribution of CD36 deficiency to this trait may be more complex to

determine. It may be worth exploring whether short-chain FA supplementation

can reverse some of the deleterious effects of CD36 deficiency in humans,

which may include hypertrophic cardiomyopathy.

* This work was supported by National Institutes of Health Grant

RO1-DK33301 (to N. A. A.), an American Heart Association Fellowship

AHA0020639T (to T. H.) and Grant AHA0030345T (to A. I.), and a grant from

the United States Department of Energy (to F. F. K).The costs of

publication of this article were defrayed in part by the payment of page

charges. The article must therefore be hereby marked " advertisement " in

accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

** To whom correspondence should be addressed: Dept. of Physiology and

Biophysics, State University of New York at Stony Brook, Stony Brook, NY

11794-8661. Tel.: ; Fax: ; E-mail:

nadaa@....