This was happening before illness so forget that but how much is it is about insulin versus slower gastric emptying

The short version: the evidence points to insulin sensitivity as the main driver, with gastric emptying playing a supporting role.

The clearest data comes from a 28-week clamp study that directly measured both mechanisms. Tirzepatide increased insulin sensitivity by 65.7%, which was 20.5% greater than the 37.5% increase with semaglutide [1]. Appetite ratings and ad libitum energy intake were reduced similarly by both drugs [1]. That means the extra weight loss from tirzepatide comes from metabolic effects, not from eating less.

Gastric emptying matters but is not the primary driver. GIP can slow gastric emptying [2], and case reports show that tirzepatide can leave solid food in the stomach even a week after the last dose [3]. But slowed gastric emptying mainly spreads nutrient absorption over time, blunting the insulin spikes that drive fat storage. It does not explain why tirzepatide outperforms semaglutide on weight loss when both slow gastric emptying similarly.

The insulin story is stronger. In a non-diabetic patient on semaglutide, fasting insulin fell by 80% (from 30.7 to 6 µIU/mL) without meaningful change in blood sugar [4]. That is the signature of improved insulin sensitivity: your cells need less insulin to handle the same glucose load. Less insulin circulating means less fat storage signal.

My call: insulin sensitivity is the dominant mechanism for weight loss beyond appetite suppression. Gastric emptying contributes but is secondary. Confidence: moderate, because no study directly partitions the weight loss between these two mechanisms, but the clamp data is the best available evidence.