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Mouse study suggests that interleukin-6 (IL-6) may regulate body weight by increasing substances in the brain that trigger weight loss. (2012) www.sciencedaily.com
From the article:
The results show that the cells that are affected by interleukin-6 produce substances that not only affect our sense of hunger and fullness but also control the body’s ability to burn fat. “Interleukin-6 increases levels of substances in the brain that trigger weight loss, which could explain why high levels of this molecule lead to weight loss,” says doctoral student Erik Schéle, who is presenting the results in his thesis.
It is known that our normally low levels of interleukin-6 in the brain increase dramatically during an infection, typically accompanied by reduced hunger and fatigue.
“Our previous findings would indicate that interleukin-6 can play a key role in regulating the metabolism of healthy individuals too,” says Erik Schéle.
“This is clearly substantiated by our finding that mice which lack interleukin-6 get fat, and that the metabolism of rats injected with interleukin-6 directly into the brain increases.”
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Hunger inhibition hormone leptin directly contributes to cardiovascular disease in those desensitized by obesity by increasing cardiovascular activity www.sciencedaily.com
From the article:
In both cell culture and animal models, the researchers have shown that fat-derived leptin directly activates aldosterone synthase expression in the adrenal glands, resulting in production of more of the steroid hormone aldosterone.
High aldosterone levels are known to contribute to widespread inflammation, blood vessel stiffness and scarring, enlargement and stiffness of the heart, impaired insulin sensitivity and more.
Aldosterone, which is produced by the adrenal gland, has a direct effect on blood pressure by regulating salt-water balance in the body. High levels of aldosterone are an obesity hallmark and a leading cause of metabolic and cardiovascular problems. But exactly how it gets high in obesity was a mystery.
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Children of women exposed to parabens during pregnancy are at greater risk of being obese. www.sciencedaily.com
Obesity is a growing problem worldwide, especially among children and young adults. Many factors contribute to obesity, including environmental exposures, which can drive epigenetic changes. Findings from a new study suggest that maternal exposure to parabens may increase the risk of obesity among children.
Parabens are widely used synthetic compounds that exert antibacterial and antifungal properties. They are commonly used in cosmetics, drugs, and some foods. Parabens can be ingested or absorbed through the skin. Some evidence suggests that parabens are endocrine disruptors.
The study had multiple arms that included an analysis of epidemiological data from the German LINA study and an experimental study in mice that simulated paraben exposure during pregnancy. The epidemiological data revealed that the children of women who had high exposure to parabens during pregnancy (assessed by urinary excretion) were more likely to be obese, an effect that was more pronounced in girls. Findings from the mouse study suggested that this increased risk of obesity was driven by epigenetic mechanisms associated with the altered expression of the proopiomelanocortin gene (known as POMC), which plays critical roles in the neuronal regulation of appetite, satiety, and food intake.
These findings suggest that prenatal environmental exposures to everyday compounds such as parabens may have far-reaching effects on the health of offspring.
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A small study found that 4 nights of sleep restriction (5hrs sleep/night) resulted in decreased satiety after a calorically dense meal. www.sciencedaily.com
A small study found that 4 nights of sleep restriction (5hrs sleep/night) resulted in decreased satiety after a calorically dense meal and altered lipid metabolism in healthy people. Catch up sleep one night only helped a little.
This was a very small study that needs to be repeated. The preliminary results found that four consecutive nights of 5 hours of sleep per night changed lipid metabolism in healthy individuals. Lipids were cleared from the bloodstream faster after a meal but they were stored in adipose tissue. This could partially explain why people did not feel satiated after a calorically dense meal.
Other studies have shown that sleep restriction also alters hormones that regulate satiety. Several studies have also shown that sleep restriction disrupts glucose metabolism. Many mechanisms may be at play.
One night of catch up sleep led to some improvements but satiety and lipid metabolism were still disrupted.