Evidence map›Paper›PMID 40585323›Full record

ArticleMetabolism open2025

Hypoglycemia compensation mechanisms in dry fasting.

Ioannis-Eleemon Papagiannopoulos-Vatopaidinos, Maria I Papagiannopoulou, Eleni N Dotsika

Abstract read
In one paragraph

Article in Metabolism open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Ioannis-Eleemon Papagiannopoulos-VatopaidinosVatopaidi Monastery Hospital, Mount Athos, 63086, Greece.
Maria I PapagiannopoulouMedical Office for Fasting Therapy, Danaidon 24a, Halandri, 15232, Greece.
Eleni N DotsikaCellular Immunology, Hellenic Pasteur Institute, Vas. Sofias Avenue 27, 11521, Greece.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Dry fasting (DF) presents three primary risks: hypovolemia, hypertonicity, and hypoglycemia. The first two have been shown to be effectively compensated, and the respective mechanisms have been studied. The behavior of glucose has only been roughly described, while the hypoglycemia compensation mechanisms remain unexplored. Objectives: Studying the glucose behavior, the hypoglycemia compensation mechanisms, and the insulin resistance during DF. Methods: Following parameters were daily monitored in ten participants undergoing a 5-day DF: Weight, body circumferences, glucose, creatinine clearance (GFR), insulin, HOMA-IR, acetoacetate in 24-h urine, glucagon, growth hormone (GH), IGF-1, TSH, T Results: Weight, body circumferences, TSH, T Conclusion: A comprehensive description of glucose behavior and the hypoglycemia compensation mechanisms in DF were presented. DF decreased insulin resistance, likely by improving the blood - cell interphase, and enhanced GFR. The increase in LDL-C, tissue-protecting IGF-1, and late increase in leptin and triglycerides were unexpected. The results may inform the development of novel therapeutic approaches for obesity, metabolic syndrome, type-2-diabetes, non-alcoholic fatty liver disease, adiposity, and atheromatous diseases.

Indexed as

Blood - Cell interphaseGFR increaseIGF-1 increase in dry fastingInsulin resistance decreaseLate leptin increase in dry fastingSelective LDL increase in dry fastingTissue protection

Identifiers

PMID40585323
PMCPMC12206320

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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.