When the front part of the liver doesn’t respond to insulin, the body makes more insulin to try to compensate.

Scientific Claim

Hepatic insulin resistance in periportal hepatocytes leads to elevated circulating insulin 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.”

From study:286-OR: Spatial Regulation of Glucose and Lipid Metabolism by Hepatic Insulin Signaling

Evidence Quality Assessment

Claim Status

appropriately stated

Study Design Support

Design supports claim

Appropriate Language Strength

definitive

Can make definitive causal claims

Assessment Explanation

Insulin levels were directly measured and reported as elevated, supporting definitive language within the context of the mouse model.

Evidence from Studies

Supporting (1)

286-OR: Spatial Regulation of Glucose and Lipid Metabolism by Hepatic Insulin Signaling

Randomized Controlled Trial

Animal

When liver cells near the entrance (periportal) stop responding to insulin, the body makes more insulin to compensate, even in mice eating a high-fat diet.

Contradicting (0)

No contradicting evidence found

Source Study

286-OR: Spatial Regulation of Glucose and Lipid Metabolism by Hepatic Insulin Signaling

Score: 10

DOI: 10.2337/db25-286-or

Similar Assertions

When the front part of the liver can't respond to insulin, blood sugar goes up—even if the liver makes less fat.

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When the part of the liver that usually responds to insulin is blocked, the liver makes less fat even when the mouse eats a high-fat diet—but its blood sugar and insulin go up instead.

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Even if you block insulin in the front part of the liver, the mouse still gets high blood sugar when eating a high-fat diet.

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The front part of the liver needs insulin to handle sugar properly when eating a high-fat diet—without it, blood sugar rises.

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The front part of the liver needs insulin to make fat when the mouse eats a lot of fat—without it, fat production drops.

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