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Most of what is known about how these two work at the mitochondria comes from laboratory and animal research, not large human trials, and there are no published human studies testing either one specifically for fatigue on a GLP-1 protocol

The timeline for clinical results with GLP-1 receptor agonists is a phased process designed to prioritize metabolic adaptation and long-term safety

That means that obesity may contribute to depression, and depression may contribute to obesity

The improved glucose metabolism is mainly due to three closely interacting factors: 1) rapid absorption of glucose from the intestine giving rise to high post-prandial glucose responses, 2) a consequent exaggerated secretion of GLP-1 that act on the -cells, and 3) radically improved hepatic and subsequently peripheral insulin sensitivity [226]

This addresses both sides of the energy balance equation: Energy in (reduced by GLP-1 and GIP appetite suppression, slower digestion) Energy out (increased by glucagon higher resting metabolic rate, enhanced fat oxidation) This dual approach may also help counteract metabolic adaptation the well-documented phenomenon where your body reduces calorie expenditure as you lose weight, which is a major reason diets and even some medications plateau