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Burn Fat Faster | How to Enter 'Fat-Burning Mode' Quicker (Pre-Fasting Strategy)
Study - American Journal of Physiology:
Assessed the impact of the macronutrient content of a meal on the postprandial leptin response. 22 young healthy subjects (11 men and 11 women) were given, in a randomized order, an isoenergetic meal [carbohydrate (81%) or fat (79%)] or remained fasting. In both genders, leptin response was higher after the carbohydrate meal than after the fat meal and while fasting. In conclusion, a carbohydrate meal induces higher postprandial leptin levels than an isoenergetic fat meal.
So we know that carbs will increase levels of leptin. However, the following study found that leptin levels need to be low in order for fat burning to take place. So trying to spike your leptin right before a fast could be counterproductive.
Leptin & Fat Burning:
To keep the human brain supplied with energy when food was scarce, mammals evolved the ability to switch from burning carbohydrates to burning fat in order to preserve skeletal muscle that would otherwise be metabolized and converted to glucose. Scientists long believed that the transition to fat metabolism was instigated solely by a drop in insulin. But a new study identified leptin as a key mediator - during starvation, plasma leptin levels fall, activating a pathway that promotes the breakdown of fat and mediates this critical shift from glucose to fat metabolism. While a drop in insulin also occurs, a decrease in leptin is also necessary for this process to happen.
Researchers investigated the rate of carbohydrate and fat metabolism as rats went from a fed to a fasted state. The researchers observed that as the rats fasted, leptin levels decreased and activated a pathway that led to fat burning rather than carb burning. During fasting, the rats' use of stored glucose went down and sugar levels decreased as a result. In turn, levels of insulin and leptin decreased - the rats' bodies then broke down body fat to be turned into ketones for energy.
Study – Cell:
Researchers had rats fast for 48 hours - plasma non-esterified fatty acid (NEFA), glycerol, and bHB (β-OHB) concentrations increased progressively throughout the fast. Unsurprisingly, the reduction in plasma glucose concentrations that occurs as a fast progresses was accompanied by reductions in plasma insulin concentrations and increases in plasma glucagon concentrations. However, they also found that plasma leptin concentrations decreased by 80% between fed and 48-hr fasted rats. Next researchers specifically investigated the impact of reductions in net hepatic glycogenolysis on rates of endogenous glucose production, plasma leptin concentrations, and activation of the HPA axis. They treated post-absorptive rats fasted for 8, 16, and 48 hour with a small molecule inhibitor of glycogen phosphorylase, which resulted in reductions in plasma glucose and insulin concentrations. This was done as it’s consistent with the negligible contributions that hepatic glycogenolysis would be expected to have on plasma glucose concentrations in the glycogen-depleted state (during prolonged fasting.) Interestingly, the reductions in plasma glucose and insulin concentrations in fasted rats treated with the glycogen phosphorylase inhibitor were associated with reductions in plasma leptin concentrations and increases in HPA axis activity, as reflected by increases in plasma corticosterone and ACTH concentrations in these groups.
The researchers next infused rats fasted for 48 hours with leptin and found:
Increased leptin levels resulted in the suppression of plasma NEFA, glycerol, β-OHB, and lactate concentrations - suppressed HPA axis activity and plasma corticosterone levels as well.
Leptin & Fat Burning:
Leptin - corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and corticosterone (cortisol in humans) concentrations. Corticotrophin-releasing hormone is secreted by the paraventricular nucleus of the hypothalamus - Corticotrophin-releasing hormone is given this name because it causes release of adrenocorticotropic hormone from the pituitary gland. Adrenocorticotropic hormone, in turn, travels in the bloodstream to the adrenal glands, where it causes the secretion of the stress hormones.