ArticleEndocrinology2013
The rise in growth hormone during starvation does not serve to maintain glucose levels or lean mass but is required for appropriate adipose tissue response in female mice.
Article in Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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.
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.
Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Treatment With a Ghrelin Agonist in Outpatient Women With Anorexia Nervosa: A Randomized Clinical Trial.The Journal of clinical psychiatryTrial
- Endocrine regulation of the hepatic fasting response: cues, cooperation and consequences.Nature reviews. Endocrinology · 2026Review
- The role of enteroendocrine cells, hormones, and gut microbiota in anorexia nervosa: a complex interplay of the microbiome-gut-brain axis.Molecular biology reports · 2025Review
- Important Hormones Regulating Lipid Metabolism.Molecules (Basel, Switzerland) · 2022Review
- Review
- Sexual dimorphic impact of adult-onset somatopause on life span and age-induced osteoarthritis.Aging cell · 2021Article
- Diverging metabolic programmes and behaviours during states of starvation, protein malnutrition, and cachexia.Journal of cachexia, sarcopenia and muscle · 2020Review
- Adipocyte JAK2 mediates spontaneous metabolic liver disease and hepatocellular carcinoma.JCI insight · 2019Article
- Low bone mineral density in anorexia nervosa: Treatments and challenges.Clinical reviews in bone and mineral metabolism · 2019Article
- Effects of Anorexia Nervosa on Bone Metabolism.Endocrine reviews · 2018Review
- Human fibroblast growth factor-21 serves as a predictor and prognostic factor in patients with hepatitis B cirrhosis combined with adrenal insufficiency.Experimental and therapeutic medicine · 2018Article
- Therapeutic effects of fibroblast growth factor‑21 against atherosclerosis via the NF‑κB pathway.Molecular medicine reports · 2018Article
- The endocrine manifestations of anorexia nervosa: mechanisms and management.Nature reviews. Endocrinology · 2017Review
- Altered somatotroph feedback regulation improves metabolic efficiency and limits adipose deposition in male mice.Metabolism: clinical and experimental · 2016Article
- Article
- Elevated GH/IGF-I promotes mammary tumors in high-fat, but not low-fat, fed mice.Carcinogenesis · 2014Article
- Anorexia nervosa and bone metabolism.Bone · 2014Review
- Determinants of GH resistance in malnutrition.The Journal of endocrinology · 2014Review
- Bone metabolism in anorexia nervosa.Current osteoporosis reports · 2014Review
- Long- but not short-term adult-onset, isolated GH deficiency in male mice leads to deterioration of β-cell function, which cannot be accounted for by changes in β-cell mass.Endocrinology · 2014Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
In mice, GH levels rise in response to short-term fasting or starvation (food restriction to 40% of ad libitum intake), similar to that which occurs in humans in response to fasting or anorexia. Recent studies using acyl-ghrelin knockout mice have suggested that the rise in GH during food restriction is essential to support glucose levels. To directly test this hypothesis, adult-onset isolated GH deficient (AOiGHD) mice and their GH-replete littermate controls were provided 40% of ad libitum food intake for 11 d. As previously shown, food restriction increased GH levels in controls, and this response was not observed in AOiGHD mice. In both controls and AOiGHD, food restriction resulted in an initial decline in glucose, which stabilized to 82-85% of ad libitum-fed values by d 2. In addition, loss of lean mass in response to food restriction was not altered by GH status. However, the loss of fat mass and the associated rise in circulating free fatty acids and ketones was blunted in starved AOiGHD mice compared with controls. Taken together, these results suggest a rise of GH during starvation is not required to support glucose levels and muscle mass but may be important in supporting fat mobilization.
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Registered trials
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.