Is saturated fat (beef tallow) a leptin analog?

Check it out;

The effect of dietary fat on diet selection may involve central
serotonin.
Mullen BJ, Martin RJ.
Department of Foods and Nutrition, University of
Georgia, Athens 30602.
Rats consuming a diet of 34% tallow select more protein and less carbohydrate than rats fed either 5% corn oil or tallow or 34% corn oil (25). To examine potential mechanism(s) of this phenomenon, we fed rats diets containing either tallow or corn oil at levels of 5 or 34% for 2 days. Sera were analyzed, and rats fed 34% tallow had higher serum insulin compared with those fed 34% corn oil. In a second experiment, rats were fed either 34% corn oil or tallow for 2 days. Brain tissues were analyzed, and rats fed 34% tallow had elevated serotonin in the raphe area compared with those fed 34% corn oil. In a third experiment, rats were fed either 34% corn oil or tallow for 2 days and then given dl-fenfluramine before diet selection. Fenfluramine depressed food intake to a greater degree in rats fed 34% tallow compared with those fed corn oil. These findings suggest that the diet selection behavior observed in tallow-fed rats may be mediated by a central serotonin system.

http://www.ncbi.nlm.nih.gov/pubmed/2600660?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=4&log$=relatedarticles&logdbfrom=pubmed


I'm kind of dorky when it comes to re-naming links. Anyways, that second link is a full study showing the effect of tallow vs corn oil on food selection. Tallow fed rats choose more protein, less carbs-- which is similar to the effects of centrally-administered leptin.


That first study mentioned fenfluramine (the fen from phen-fen.)

Look what wikipedia says;

The drug was withdrawn from the U.S. market in 1997 after reports of heart
valve disease,[2][3] and pulmonary hypertension, including a condition known as cardiac fibrosis. After the US withdrawal of fenfluramine, it was also withdrawn from other markets around the world.
The distinctive valvular abnormality seen with fenfluramine is a thickening of the leaflet and chordae tendineae. One mechanisms used to explain this phenomenon involves heart valve serotonin receptors, which are thought to help regulate growth. Since fenfluramine and its active metabolite norfenfluramine stimulate serotonin receptors 5-hydroxytryptamine (5-HT) this may have led to the valvular abnormalities found in patients using fenfluramine. In particular norfenfluramine is a potent agonist of 5-HT2B receptors, which are plentiful in human cardiac valves. The suggested mechanism by which fenfluramine causes damage is through over or inappropriate stimulation of these receptors leading to inappropriate valve cell division. Supporting this idea, is the fact that this valve abnormality has also occurred in patients using other drugs that act on 5-HT2B receptors. [4].

I really haven't done enough homework to say this; but I'm gonna say it anyways. Heart disease is a disease of energy homeostasis; largely mediated by serotonin. Overgrowth, thickening of the arteries perhaps caused by overactive serotonin receptors; or undergrowth, leaky artery disease not all that far removed from leaky gut disease, since the gut is also dependent on serotonin for the mediation of its upkeep.

Edit; make that involving serotonin. Then toss that whole last paragraph over your shoulder.

Back on topic. Or as close as I'm capable.

http://www.ncbi.nlm.nih.gov/pubmed/11540865

d-Fenfluramine selectively suppresses carbohydrate snacking by obese
subjects.
Wurtman J, Wurtman R, Mark S, Tsay R, Gilbert W, Growdon J.
Department of Applied Biology, MIT, Cambridge, MA
02139, USA.
Twenty obese inpatients who claimed to crave carbohydrate-rich foods were given d-fenfluramine (15 mg p.o., twice daily) or its placebo, double-blind, for two consecutive eight-day periods. Food choices were measured on treatment days 1, 7, and 8 by giving the subjects access to unlimited portions of six isocaloric meal foods (three high in carbohydrate and three high in protein) and of 10 isocaloric snack foods (five high in protein and five high in carbohydrate) available 24 hours a day in a computerized vending machine. d-fenfluramine reduced mealtime calorie intake by only 16% (from 1940 +/- 94 to 1630 +/- 92; p < .001), mealtime carbohydrate by 22%, and had no significant effect on mealtime protein consumption; in contrast, snack calorie intake was reduced by 41% (from 707 +/- 97 to 414 +/- 46; p < .001), and snack carbohydrate intake by the same proportion. The mean number of carbohydrate-rich snacks consumed per day decreased from 5.8 +/- 0.8 to 3.4 +/-0.4 (p < .01), while that of protein-rich snacks failed to change signficantly (i.e., from 0.7 +/- 0.2 to 0.5 +/- 0.2).

Tallow-fed rats already had blunted carbohydrate appetites. Fenfluramine "satisfies" carbohydrate appetite, perhaps by sending the false signal that carbohydrates have already been eaten; so fenfluramine ends up more effective for tallow fed than for corn oil fed rats. A false signal of nourishment might not be a good idea.