Leptin and the Control of Body Weight: A Review of Its Diverse Central Targets, Signaling Mechanisms, and Role in the Pathogenesis of Obesity

I just read the paper Leptin and the Control of Body Weight: A Review of Its Diverse Central Targets, Signaling Mechanisms, and Role in the Pathogenesis of Obesity

It is mostly a review of the details of what is known about how leptin fits into the system of energy homeostasis. There were a couple of things that caught my attention. One is that high triglyceride levels cause the leptin system to think it is detecting starvation:

Several factors
have been identified to influence the
rate of leptin transport into the CNS.
α-Adrenergic stimulation for example
increases transporter activity (35),
whereas hypertriglyceridemia markedly
impairs it (36). Hypertriglyceridemia
is generally observed during prolonged
starvation and it is hypothesized that
the ability of triglycerides to inhibit leptin
transport may have in part arisen as
an evolutionary mechanism to counteract
the propagation of anorexic signals
during food shortage.
hypertriglyceridemia is also associated
with obesity and may in part be
responsible for the impairment of leptin
transport that is observed in obese
individuals and defines the condition
of peripheral leptin resistance (32–34).
Peripheral resistance like central resistance
is both a cause and a consequence
of obesity, meaning that the two types
of resistance are likely to co-exist and
once established set off a vicious cycle of
weight gain

There is a food that is common in present day America that is uniquely good at causing high triglyceride levels -- fructose. See for example, Fructose: Metabolic, Hedonic, and Societal Parallels with Ethanol, in the section titled DNL. DNL is an acronym for de novo lipogenesis, which is fat that the body makes out of carbohydrates.

 DNL is markedly
increased by excess dietary CHO, rather than excess dietary
fat (78). For example, if total CHO energy intake
exceeds total energy expenditure, hepatic DNL is incremented
10-fold (79). Similarly, on a high-CHO diet, DNL
synthesis is 27 times increased in the fasting state as
compared with a low-CHO diet, and 4 times increased in
the fed state (80). Fructose is a primary driver of DNL.
Human studies demonstrate a rate of fractional DNL of
2% with glucose and 10% after 6 days of high-fructose
feeding (81,82) A recent human study demonstrated that
fructose feeding increased fractional DNL to 17% (83).

In other words, this adds up to strong evidence that eating high levels of foods made with table sugar and/or HCFS will disrupt the energy homeostasis in the body, causing the body to think it is starving and hence, driving excessive eating.

The other piece of suggestive information in the leptin article is that leptin ties into learning in the brain. The authors don't say this, but it is easy to imagine that what is happening is that the brain takes special note of the foods it is eating when it thinks it is starving and turns on what is called the hedonic reward system. In other words, the brain "decides" it really likes foods it eats when it thinks it is starving.

It's easy to see this as part of plants grand scheme to get their genes (seeds) transported far and wide. By producing high levels of a food that causes the animals to eat it to want more of it, the plants encourage the animals to eat as much as they can -- thus carrying the payload (from the plants point of view) far from the plant mother ship, where the baby plants have a better chance to grow and spread.