When the front part of the liver can't respond to insulin, blood sugar goes up—even if the liver makes less fat.
Scientific Claim
Hepatic insulin resistance in periportal hepatocytes leads to elevated blood glucose levels in mice on a high-fat diet.
Original Statement
“PP-insulin resistance in mice impaired lipogenesis and suppressed high-fat diet (HFD)-induced hepatosteatosis, despite elevating blood glucose and insulin.”
Evidence Quality Assessment
Claim Status
appropriately stated
Study Design Support
Design supports claim
Appropriate Language Strength
definitive
Can make definitive causal claims
Assessment Explanation
Blood glucose was quantitatively measured and reported as elevated, supporting definitive language within the mouse model context.
Evidence from Studies
Supporting (1)
286-OR: Spatial Regulation of Glucose and Lipid Metabolism by Hepatic Insulin Signaling
When liver cells near the entrance (periportal) stop responding to insulin, blood sugar goes up—even if the liver makes less fat. This study proved it in mice on a high-fat diet.