A fellow commenter (Westie) on Peter's Hyperlipid Blog told me this;

Glutamine decreases the amount of glucose carbon directed to Krebs cycle. That
is connected to increased UCP-2 expression which is also related to insulin
resistance.

This single sentence explains quite a bit of the stuff I've been reading about leptin. I might as well start here, it's as good as anywhere;
http://cmbi.bjmu.edu.cn/news/report/2009/pdf/med09_09_1.pdf

Leptin inhibition of bone mass accrual requires the integrity of specific hypothalamic neurons but not expression of its receptor on these neurons. The same is true for its regulation of appetite and energy expenditure. This suggests that leptin acts elsewhere in the brain to achieve these three functions.We show here that brainstem-derived serotonin (BDS) favors bone mass accrual following its binding to Htr2creceptors on ventromedial hypothalamic neurons and appetite via Htr1a and 2b receptors on arcuate neurons. Leptin inhibits these functions and increases energy expenditure because it reduces serotonin synthesis and firing of serotonergic neurons. Accordingly,while abrogating BDS synthesis corrects the bone, appetite and energy expenditure phenotypes caused by leptin deficiency,inactivation of the leptin receptor in serotonergic neurons recapitulatesthem fully. This study modifies the map of leptin signaling in the brain andidentifies a molecular basis for the common regulation of bone and energymetabolisms.

The authors mention later on that leptin shows up with skeletons, so it makes sense that it is involved in proper bone mass maintenance. So leptin has a very close relationship to serotonin. I'm going to skip over serotonin for now, mostly because while I know that serotonin is involved in appetite and metabolism etc., all over the body, that's about all I know, and I came here to talk about leptin.
Okay, into the meat of the thing.
http://endo.endojournals.org/cgi/content/full/145/2/839
Leptin decreases the preference for the taste of sweet.
http://ajpregu.physiology.org/cgi/content/full/293/4/R1468

Leptin reduces body fat selectively, sparing body protein. Accordingly, during chronic leptin administration, food intake is suppressed, and body weight is
reduced until body fat is depleted. Body weight then stabilizes at this fat-depleted nadir, while food intake returns to normal caloric levels, presumably in defense of energy and nutritional homeostasis. This model of leptin treatment offers the opportunity to examine controls of food intake that are independent of leptin's actions, and provides a window for examining the nature of feeding controls in a "fatless" animal. Here we evaluate macronutrient selection during this fat-depleted phase of leptin treatment. Adult, male Sprague-Dawley rats were maintained on standard pelleted rodent chow and given daily lateral ventricular injections of leptin or vehicle solution until body weight reached the nadir point and food intake returned to normal levels. Injections were then continued for 8 days, during which rats self-selected their daily diet from separate sources of carbohydrate, protein, and fat. Macronutrient choice differed profoundly in leptin and control rats. Leptin rats exhibited a dramatic increase in protein intake, whereas controls exhibited a strong carbohydrate preference. Fat intake did not differ between groups at any time during the 8-day test. Despite these dramatic differences in macronutrient selection, total daily caloric intake did not differ between groups except on day 2. Thus controls of food intake related to ongoing metabolic and nutritional requirements may supersede the negative feedback signals related to body fat stores.

This study has sort of confused me for a while; leptin decreases the appetite for carbohydrate. But, isn't the alternate fuel fat, not protein? But if you throw in this;

Glutamine decreases the amount of glucose carbon directed to Krebs cycle

Then gosh, glutamine becomes awfully important to the switch between glucose and fat as the major energy source.
We taste sweet, sour, bitter, salty, umami. Umami is the taste set off by mono-sodium glutamate. We taste glutamine, glutamic acid, etc. Out of all the proteins we have a particular sense of taste for that one protein.
Yeah, I know. MSG makes you fat, right? But... l glutamine is often recommended to fight carbohydrated addiction. Also alcohol addiction.
And there's this; http://www.ncbi.nlm.nih.gov/pubmed/18559279?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=2&log$=relatedarticles&logdbfrom=pubmed

Monosodium l-glutamate (MSG), an umami taste substance, may be a key molecule coupled to a food intake signaling pathway, possibly mediated through a specific l-glutamate (GLU) sensing mechanism in the gastrointestinal tract. Here we investigated the effect of the spontaneous ingestion of a 1% MSG solution and water on food intake and body weight in male Sprague-Dawley rats fed diets of varying caloric density, fat and carbohydrate contents. Fat mass and lean mass in the abdomen, blood pressure, and several blood metabolic markers were also measured. Rats given free access to MSG and water showed a high preference (93-97%) for the MSG solution, regardless of the diet they consumed. Rats ingesting MSG had a significantly smaller weight gain, reduced abdominal fat mass, and lower plasma leptin levels, compared to rats ingesting water alone. Naso-anal length, lean mass, food and energy intakes, blood pressure, blood glucose, and plasma levels of insulin, triglyceride, total cholesterol, albumin, and GLU were not influenced by the ingestion of the MSG solution. These same effects were observed in a study of adult rats. Together, these results suggest that MSG ingestion reduces weight gain, body fat mass, and plasma leptin levels. Moreover, these changes are likely to be mediated by increased energy expenditure, not reduced energy intake or delayed development. Conceivably, these effects of MSG might be mediated via gut GLU receptors functionally linked to afferent branches of the vagus nerve in the gut, or the afferent sensory nerves in the oral cavity.

Pay special attention to those red letters. Looking for this study, I sorted through a someshort term studies in humans. One bowl of soup containing lots of msg, followed by a meal, failing to suppress appetite. That doesn't matter. Another important thing to note; the rats drank msg-water or msg-free water at will; the rat's natural appetites were in charge. MSG mixed into chow would be an entirely different experiment.

Of course, I'm not dismissing possible consequences of individual MSG sensitivities, I really don't know enough about that stuff to even comment.

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Okay. Leptin and fat accumulation.
http://ajpendo.physiology.org/cgi/content/full/285/3/E521

To test whether fatty acids play a messenger role between stimulation of lipolysis by norepinephrine and inhibition of leptin secretion, adipocytes were incubated with insulin (10 nM) in the presence of norepinephrine (1 µM) or palmitic acid (1 mM; Fig. 1). Because albumin strongly binds extracellular fatty acids (4), experiments were carried out at low (0.1%) and high (4%) albumin concentrations. Palmitic acid (1 mM) mimicked the inhibitory effects of norepinephrine (1 µM) on leptin secretion at low but not at high albumin concentrations (Fig. 1). This indicates that albumin, at high concentrations, effectively binds extracellular fatty acids and consequently inhibits their effects on leptin secretion. Therefore, subsequent experiments were carried out at low albumin concentrations. Concentration-response curves carried out in the presence of 0.1% albumin revealed that palmitic acid inhibited insulin (10 nM)-stimulated leptin secretion between 0.1 and 1 mM without significantly affecting basal values (Fig. 2). In fact, the palmitic acid effect critically depended on the ratio of the molar concentrations of palmitic acid over albumin with an IC50 of 4.5 (Fig. 3). This is consistent with the observation that one molecule of albumin has several low- and high-affinity binding sites for long-chain fatty acids

The fact that concentrations of albumin similar to those found in plasma (4%) inhibit the effects of palmitic acid (1 mM) indicates that circulating fatty acids (the concentration of which varies at the millimolar level) have little influence on leptin secretion, at least directly (Figs. 1 and 3). This is supported by several in vivo studies in humans, which failed to demonstrate any inhibitory effects of fatty acids on plasma leptin concentrations (35, 37). It is more likely that an intracellular increase in fatty acids, generated in consequence of activated lipolysis, causes the inhibition of leptin secretion

When the fat cell is awash in free fatty acids, particularly palmitic acid, but not in albumin, leptin secretion is suppressed. When would lipolysis be high? I'd assume that lipolysis is high inside the fat cell at the same times that it's high in other parts of the body, like the liver. When fat is being used for energy. When is fat being used for energy?
1) when carbs are low
2) when all the tools necessary to the efficient use of fat for energy are present.

Glutamine decreases the amount of glucose carbon directed to Krebs cycle. That
is connected to increased UCP-2 expression which is also related to insulin
resistance.

Here's an interesting thing;

http://ajpendo.physiology.org/cgi/content/full/289/1/E166

Amino acids are catabolized at the glycolysis and tricarboxylic acid cycle levels (Table 1). Interestingly, they exhibited the following four different types of effect on leptin secretion: 1) amino acids that stimulated poorly or did not stimulate leptin secretion (L-glycine, L-alanine, L-histidine, L-arginine and L-glutamine; Figs. 3 and 6), 2) an amino acid that increased leptin secretion only in the presence of glucose (L-leucine; Fig. 4), 3) an amino acid that mimicked and potentiated glucose action (L-aspartate, L-valine, L-methionine, and L-phenylalanine; Figs. 4 and 5), and 4) an amino acid that stimulatedleptin secretion in the absence of glucose or insulin (L-glutamate]; Fig. 4). Each of these is discussed below

Glutamic acid was special in this study in that it stimulated leptin secretion in the absence of glucose or insulin. Hunger for protein increases after fat depletion in leptin-treated Sprague-Dawley rats. Glutamic acid is the one protein we have specific taste-receptors for, the taste "umami."
Another interesting line in that study;

First, regarding the amino acids that did not show any or showed only small effects on leptin secretion, one hypothesis is that white adipocytes metabolize these amino acids poorly. For example, glutamine is known to be released rather than being oxidized in white adipose tissue.

What, the same adipose tissue that's famous for releasing leptin when glutamic acid is present, even in a low-insulin, low-glucose state? Could leptin help fat cells synthesize glutamine from glutamic acid?
Maybe.
http://www.nature.com/ijo/journal/v23/n11/abs/0801095a.html

However, in the presence of leptin, the production of glucose from glycerol (2 mM), L-lactate (2 mM). L-alanine (5 mM) and L-glutamine (5 mM) by the isolated hepatocytes was significantly reduced (30%, 30%, 23% and 25%, respectively).

Well, it looks like I was in the ballpark, anyways. The reduction of glucose production from L-glutamine would at least increase local glutamine levels. So glutamic acid increases leptin production, and leptin decreases attrition of glutamine to glucose synthesis.