Evidence map›Paper›PMID 29244064›Full record

ArticleEndocrinology2018

β-Cell Control of Insulin Production During Starvation-Refeeding in Male Rats.

Brandon B Boland, Charles Brown, Cristina Alarcon, Damien Demozay, Joseph S Grimsby, Christopher J Rhodes

Abstract read
In one paragraph

Article in Endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed.

  1. Article
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  9. Supplementary Effects ofPharmaceuticals (Basel, Switzerland) · 2023
    Article
  10. Article
  11. Article
  12. SIRT6 regulates SREBP1c-induced glucolipid metabolism in liver and pancreas via the AMPKα-mTORC1 pathway.Laboratory investigation; a journal of technical methods and pathology · 2022
    Article
  13. Review
  14. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Brandon B BolandKovler Diabetes Center, Department of Medicine Section of Endocrinology, Diabetes and Metabolism, University of Chicago, Chicago, Illinois.
Charles BrownDivision of Cardiovascular and Metabolic Disease, MedImmune LLC, Gaithersburg, Maryland.
Cristina AlarconKovler Diabetes Center, Department of Medicine Section of Endocrinology, Diabetes and Metabolism, University of Chicago, Chicago, Illinois.
Damien DemozayKovler Diabetes Center, Department of Medicine Section of Endocrinology, Diabetes and Metabolism, University of Chicago, Chicago, Illinois.
Joseph S GrimsbyDivision of Cardiovascular and Metabolic Disease, MedImmune LLC, Gaithersburg, Maryland.
Christopher J RhodesKovler Diabetes Center, Department of Medicine Section of Endocrinology, Diabetes and Metabolism, University of Chicago, Chicago, Illinois.

Funding

TRANSGENIC COREP60DK020595 · NIDDK · UNIVERSITY OF CHICAGO · PI BELL, GRAEME I · 1985 to 2012
$25.5M
Pilot and Feasibility ProgramP30DK020595 · NIDDK · UNIVERSITY OF CHICAGO · PI Matthew J Brady · 2013 to 2026
$20.9M
METABOLIC CONTROL PROINSULIN BIOSYNTHESIS TRANSLATIONR01DK050610 · NIDDK · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI RHODES, CHRISTOPHER J · 1996 to 2014
$5.1M
Central Control of Pancreatic Islet FunctionR01DK099359 · NIDDK · UNIVERSITY OF CHICAGO · PI RHODES, CHRISTOPHER J · 2015 to 2018
$1.9M
NIDDK NIH HHS P30 DK020595NIDDK NIH HHS P60 DK020595NIDDK NIH HHS R01 DK050610NIDDK NIH HHS R01 DK099359
6 · The paper itself

Abstract

Mammalian metabolism has evolved to adapt to changes in nutrient status. Insulin, the key anabolic hormone, facilitates intracellular storage of nutrient fuels and plays a pivotal role in the transition away from catabolism upon refeeding. Although circulating insulin relative to nutrient levels has been well characterized during fasting and refeeding, how pancreatic β-cell biology caters to acute changes in insulin demand has not been sufficiently addressed. Here, we examined the dynamics of (pro)insulin production and associated changes in β-cell ultrastructure during refeeding after a 72-hour fast in male rats. We found that fasted β-cells had marked degranulation, which inversely coordinated with the upregulation of autophagolysomal and lysosomal organelles. There was also expanded Golgi that correlated with enhanced (pro)insulin biosynthetic capacity but, conversely, blunted in vivo insulin secretion. Within 4 to 6 hours of refeeding, proinsulin biosynthesis, cellular ultrastructure, in vivo insulin secretion, and glucose tolerance normalized to levels near those of fed control animals, indicating a rapid replenishment of normal insulin secretory capacity. Thus, during a prolonged fast, the β-cell protects against hypoglycemia by markedly reducing insulin secretory capacity in vivo but is simultaneously poised to efficiently increase (pro)insulin production upon refeeding to effectively return normal insulin secretory capacity within hours.

Indexed as

AnimalsCells, CulturedEatingFastingInsulinInsulin-Secreting CellsMaleRatsRats, WistarStarvationInsulin

Identifiers

PMID29244064
PMCPMC5776497

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.