When mice lack the AMPKα1 gene, their kidneys handle salt normally and produce less urine than usual.

Scientific Claim

Mice with AMPKα1 knockout exhibit normal renal sodium handling and a moderate antidiuretic state.

Original Statement

“AMPKα1 knockout (KO) mice exhibit normal renal sodium handling and a moderate antidiuretic state.”

Claim Status

appropriately stated

Study Design Support

Design supports claim

Appropriate Language Strength

definitive

Can make definitive causal claims

Assessment Explanation

The abstract directly states the observation using 'exhibit', which is appropriate for a descriptive claim in an animal model.

Kidney-specific genetic deletion of both AMPK α-subunits causes salt and water wasting.

Cohort Study

Animal

2017 Feb 1

No contradicting evidence found

When mice lose both AMPKα1 and AMPKα2 in their kidneys, they lose too much water and salt in their urine.

84%

In mice, AMPK is linked to how the kidneys function.

81%

Mice missing the AMPKα1 gene produce more aldosterone in their urine and have lower blood pressure than normal mice.

77%