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Hypothalamic resistin induces hepatic insulin resistance

2007· article· en· 116 citations· W2016248729 on OpenAlex· 10.1172/jci30440

Why is this work in the frame?

A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

Canadian affiliationAn author listed a Canadian institution. This is the only route the usual frame has.
Canadian funderA Canadian agency funded it. The work may carry no Canadian affiliation at all.

The three-model screen

all 1,000 screened works →

All three models called this out of scope.

stratum: aff_core · design weight: 5595.24 (the sample is stratified; any rate computed without the weight is wrong)
Claude Opus 4.8OUT
genre: empirical
about Canada: no
confidence: high

Physiology study of hypothalamic resistin and hepatic insulin resistance; the object is a metabolic mechanism.

GPT-5.6 (high)OUT
genre: empirical
about Canada: no
confidence: high

The study investigates hypothalamic resistin and insulin resistance, not research practice.

Grok 4.5OUT
genre: empirical
about Canada: no
confidence: high

Physiology study of hypothalamic resistin and insulin resistance; biomedical domain.

Abstract

Circulating resistin stimulates endogenous glucose production (GP). Here, we report that bi-directional changes in hypothalamic resistin action have dramatic effects on GP and proinflammatory cytokine expression in the liver. The infusion of either resistin or an active cysteine mutant in the third cerebral ventricle (icv) or in the mediobasal hypothalamus stimulated GP independent of changes in circulating levels of glucoregulatory hormones. Conversely, central antagonism of resistin action markedly diminished the ability of circulating resistin to enhance GP. We also report that centrally mediated mechanisms partially control resistin-induced expression of TNF-alpha, IL-6, and SOCS-3 in the liver. These results unveil what we believe to be a novel site of action of resistin on GP and inflammation and suggest that hypothalamic resistin action can contribute to hyperglycemia in type 2 diabetes mellitus.

Stored with the screening record, where it is evidence for the labels above.

The record

Venue
Journal of Clinical Investigation
Topic
Adipokines, Inflammation, and Metabolic Diseases
Field
Medicine
Canadian institutions
University Health Network
Funders
National Institute of Diabetes and Digestive and Kidney DiseasesNational Cancer InstituteUniversity of TorontoNational Institutes of HealthAmerican Diabetes Association
Keywords
ResistinInternal medicineEndocrinologyInsulin resistanceProinflammatory cytokineHypothalamusMedicineInsulinHormoneInflammationAdipokine
Has abstract in OpenAlex
yes