A high-dose intravenous infusion of arginine vasopressin raises blood glucose levels by about 0.8 mmol/L in healthy adults without changing insulin levels, and this increase is caused by glucagon triggering the breakdown of glycogen in the liver.
See the scientific wording
Supraphysiological intravenous infusion of arginine vasopressin (AVP) at 112.3 pmol/L increases plasma glucose by approximately 0.8 mmol/L in healthy adults without altering insulin, and this effect is mediated by glucagon-mediated glycogenolysis in the liver.
Correlational — new studies may shift this
One low-scoring study links this claim to the outcome, but causation is not established.
What the research says
1 study reviewedSupporting (1)
Hydration, Arginine Vasopressin, and Glucoregulatory Health in Humans: A Critical Perspective
Narrative ReviewReview2019
When scientists injected a high dose of the hormone AVP into people’s veins, their blood sugar went up by about 0.8 mmol/L — just like the claim says. This happened because AVP triggered the liver to release stored sugar, likely through another hormone called glucagon.
Contradicting (0)
No contradicting studies found yet
That doesn't mean it's settled — it just means no study has tested the opposite.
Quality-weighted scoring: we follow the GRADE framework — each study is rated High, Moderate, Low, or Very Low based on study design, methodology rigor, and risk of bias. A single high-quality RCT can outweigh several weaker observational studies.
Scores reflect study quality, not just count.
A high dose of the hormone AVP binds to receptors on pancreatic cells that produce glucagon, causing those cells to release more glucagon. The glucagon then travels to the liver and triggers the breakdown of stored sugar into glucose, which is released into the blood, raising blood sugar levels without changing insulin.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting study
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A high-dose intravenous infusion of arginine vasopressin raises blood glucose levels by about 0.8 mmol/L in healthy adults without changing insulin levels, and this increase is caused by glucagon triggering the breakdown of glycogen in the liver.
Mechanism
1 studyA high dose of AVP tells the pancreas to release more glucagon, which tells the liver to break down its sugar stores and dump glucose into the blood. This raises blood sugar without changing insulin. Other possible ways to raise blood sugar, like dehydration or stress hormones, do not occur under these specific conditions.
A high dose of the hormone AVP binds to receptors on pancreatic cells that produce glucagon, causing those cells to release more glucagon. The glucagon then travels to the liver and triggers the breakdown of stored sugar into glucose, which is released into the blood, raising blood sugar levels without changing insulin.
Arginine vasopressin is infused into the bloodstream at supraphysiological concentrations, reaching plasma levels of 112.3 pmol/L.
Arginine vasopressin binds to V1 receptors on pancreatic alpha cells, activating intracellular signaling that stimulates glucagon secretion.
Elevated glucagon binds to receptors on hepatocytes, activating cAMP-PKA signaling that triggers the breakdown of glycogen into glucose.
Hepatic glucose output increases, raising arterialized-venous plasma glucose concentrations by approximately 0.8 mmol/L without altering insulin secretion or glucose disposal.
Less supported by current evidence, but not ruled out
A sharp increase in blood salt concentration causes liver cells to lose water, which directly triggers the release of glucagon and the breakdown of stored sugar into glucose.
Hypertonic solutes increase extracellular osmolality, causing water to exit hepatocytes and inducing cellular shrinkage.
Hepatocyte shrinkage activates intracellular signaling pathways that stimulate glucagon secretion from pancreatic alpha cells.
Glucagon increases hepatic glycogenolysis, elevating plasma glucose without changes in insulin.
Severe fluid loss increases stress hormones glucagon and cortisol, which together force the liver to release more glucose into the blood.
Hypohydration reduces blood volume and increases plasma osmolality, activating stress responses.
Glucagon secretion increases, stimulating hepatic glycogenolysis.
Cortisol secretion increases, enhancing gluconeogenesis and hepatic glucose output.
Combined glucagon and cortisol actions elevate plasma glucose independently of insulin changes.
Evidence from Studies
Supporting (1)
Community contributions welcome
Hydration, Arginine Vasopressin, and Glucoregulatory Health in Humans: A Critical Perspective
When scientists injected a high dose of the hormone AVP into people’s veins, their blood sugar went up by about 0.8 mmol/L — just like the claim says. This happened because AVP triggered the liver to release stored sugar, likely through another hormone called glucagon.
Contradicting (0)
Community contributions welcome
Score Breakdown
No multi-axis breakdown available yet. The overall Pro / Against score above is the best signal.
- No clinical evidence is available; the score reflects mechanistic plausibility only.
What Would Prove This
Per GRADE and EBM methodology, here is what ideal scientific evidence would look like to definitively prove or disprove this claim, ordered from strongest to weakest.
Systematic Review of Intravenous AVP Infusion Effects on Glucose Metabolism in Healthy Adults
Population: Healthy adults; Intervention: Supraphysiological IV AVP at 112.3 pmol/L; Comparator: Saline placebo; Outcome: Change in plasma glucose and insulin levels; Duration: Single infusion with measurements at 0, 15, 30, 60, and 120 minutes
Double-Blind RCT of AVP vs Saline on Hepatic Glucose Output in Healthy Adults
Population: Healthy adults; Intervention: IV AVP at 112.3 pmol/L; Comparator: IV saline; Outcome: Plasma glucose, insulin, glucagon, and hepatic glucose production measured by tracer methodology; Duration: Single infusion over 120 minutes
Prospective Cohort of Healthy Adults Receiving AVP Infusion to Monitor Glucose and Glucagon Dynamics
Population: Healthy adults; Intervention: IV AVP at 112.3 pmol/L; Comparator: None (single-arm); Outcome: Serial measurements of plasma glucose, insulin, glucagon, and glycogenolysis markers; Duration: 120 minutes post-infusion
Human Hepatocyte Culture Exposed to AVP to Measure Glycogenolysis and Glucagon Receptor Activation
Population: Primary human hepatocytes; Intervention: AVP at 112.3 pmol/L; Comparator: Vehicle control; Outcome: Glycogen content, glucagon receptor phosphorylation, glucose output; Duration: 60–120 minutes
Rodent Model of AVP Infusion to Assess Hepatic Glucose Production and Glucagon Dependence
Population: Healthy adult rodents; Intervention: IV AVP at 112.3 pmol/L; Comparator: Saline; Outcome: Blood glucose, liver glycogen, glucagon levels, and hepatic enzyme activity; Duration: 90 minutes post-infusion