Dr. Benjamin Bikman

Dr. Benjamin Bikman, a Brigham Young University metabolic researcher, explains the mechanistic case for allulose — a rare sugar that does not appear to spike insulin and may activate GLP-1 and AMPK pathways. Replacing fructose with allulose may reduce uric acid production in mechanistic models, with potential downstream effects on insulin sensitivity, fat oxidation, and possibly brain ketone availability. The episode is mechanism-rich and the substitution argument is biologically plausible; large clinical-outcome trials remain limited, so the practical framing is sweetener-of-choice for people who already use sweeteners, not a stand-alone metabolic intervention.

Insulin resistance may sit under several chronic conditions, and lowering insulin can support fat burning. The carbohydrate-insulin model adds nuance to the calorie-balance view rather than replacing it. The strongest practical levers are not exotic: lower-carb whole foods, more protein, strength training, and meal timing.

Most weight-loss talk focuses on insulin, but its partner hormone, glucagon, is getting new attention. Glucagon is one of the key hormones that helps keep fuel available when you are not eating: it mainly acts on the liver, telling it to release stored glucose and, in the right conditions, to burn fat and make ketones. Because it can raise fat burning and energy use in the liver, some experimental obesity drugs are being designed to add a glucagon effect on top of GLP-1. It is a genuinely interesting piece of metabolism, but not a switch most people need to manage themselves.