Metformin is a biguanide, a class of drugs that aid in glucose disposal. Metformin decreases blood glucose levels by reduced gluconeogenesis (liver), decreased glucose absorption (intestines), and increasing insulin sensitivity (liver) by increasing glucose uptake and utilization.
While it seems a popular idea that Met increases skeletal muscle insulin sensitivity (which would be great for muscle anabolism), the primary site of its insulin sensitizing effects is the liver. Its actions on skeletal muscle is actually quite negative: it inhibits mTOR complex 1 (protein synthesis, translation) thereby reducing hypertrophy; it blocks the preferential shift from type I to type IIA fibers (resulting in a tendency towards reduced strength gains); and blocks the endurance training (LISS, HIIT, cardio) enhancement of insulin sensitivity. When Metformin alone is compared to a progressive resistance training program alone in older sedentary people, its effects (on blood glucose levels & absorption, insulin sensitivity) are indistinguishable from the resistance training program alone; and Metformin + progressive resistance training does worse than either Metformin with no training and/or resistance training alone.
Insulin (exogenous) promotes the uptake & utilization of glucose from the blood into skeletal muscle, repleting glycogen, enhancing insulin sensitivity in skeletal muscle. Rather than blunting fat synthesis & promoting fat oxidation like Metformin (another of Met's effects), it does the opposite
potently, and dramatically increases VLDL synthesis in the liver (increasing the most dangerous particles for cardiovascular risks). Over time at high doses, it worsens insulin sensitivity by diminished autophosphorylation of the IR & its downstream elements, thereby reducing this skeletal muscle uptake of glucose and logically (though it has not been demonstrated insofar as I am aware) the muscle protein anabolic effects. See
Insulin’s effects and mechanisms in promoting skeletal muscle hypertrophy, November 17, 2022, Type-IIx MesoRx Article
While the two drugs (Met & slin) may be used in diabetic patients, it requires dose reductions, and this is further complicated by AAS (that increase insulin sensitivity in skeletal muscle). Since slin so potently overwhelms the effects of Met and they act oppositely in some key ways, this should be considered before combining the two. A potential very high severity outcome is hypoglycemic shock, coma, and death.