Home › Research › Drug development
Milk signalling in the pathogenesis of type 2 diabetes
Melnik BC.. Medical hypotheses, 2011-01-19
Topic: Brain proteins, microglia and lab models
The presented hypothesis identifies milk consumption as an environmental risk factor of Western diet promoting type 2 diabetes (T2D). Milk, commonly regarded as a valuable nutrient, exerts important endocrine functions as an insulinotropic, anabolic and mitogenic signalling system supporting neonatal growth and development. The presented hypothesis substantiates milk's physiological role as a signalling system for pancreatic β-cell proliferation by milk's ability to increase prolactin-, growth hormone and incretin-signalling. The proposed mechanism of milk-induced postnatal β-cell mass expansion mimics the adaptive prolactin-dependent proliferative changes observed in pregnancy. Milk signalling down-regulates the key transcription factor FoxO1 leading to up-regulation of insulin promoter factor-1 which stimulates β-cell proliferation, insulin secretion as well as coexpression of islet amyloid polypeptide (IAPP). The recent finding that adult rodent β-cells only proliferate by self-duplication is of crucial importance, because permanent milk consumption beyond the weaning period may continuously over-stimulate β-cell replication thereby accelerating the onset of replicative β-cell senescence. The long-term use of milk may thus increase endoplasmic reticulum (ER) stress and toxic IAPP oligomer formation by overloading the ER with cytotoxic IAPPs thereby promoting β-cell apoptosis. Both increased β-cell proliferation and β-cell apoptosis are hallmarks of T2D. This hypothesis gets support from clinical states of hyperprolactinaemia and progeria syndromes with early onset of cell senescence which are both associated with an increased incidence of T2D and share common features of milk signalling. Furthermore, the presented milk hypothesis of T2D is compatible with the concept of high ER stress in T2D and the toxic oligomer hypothesis of T2D and may explain the high association of T2D and Alzheimer disease.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Melnik, B. C. (2011). Milk signalling in the pathogenesis of type 2 diabetes. Medical hypotheses. https://doi.org/10.1016/j.mehy.2010.12.017
Vancouver
Melnik BC. Milk signalling in the pathogenesis of type 2 diabetes. Medical hypotheses. 2011. doi:10.1016/j.mehy.2010.12.017. PMID: 21251764.
BibTeX
@article{melnik2011-21251764,
author = {Melnik, B. C.},
title = {{Milk signalling in the pathogenesis of type 2 diabetes}},
journal = {Medical hypotheses},
year = {2011},
doi = {10.1016/j.mehy.2010.12.017},
pmid = {21251764},
url = {https://doi.org/10.1016/j.mehy.2010.12.017}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- This hypothesis gets support from clinical states of hyperprolactinaemia and progeria syndromes with early onset of cell senescence which are both associated with an increased incidence of T2D and share common features of milk signalling.
New to this subject? Start with our plain-English guide: Treatments →
Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multicenter collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Medical hypotheses) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2011 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 21251764) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
Free copy unknown: no free-copy check has an answer for this record yet. That does not mean it is paywalled.
Related
Studies in the library that share something with this one. The line above each title says what.
Related studies in Drug development
Also tagged “pathogenesis”
5 studies in the library carry the topic tag “pathogenesis”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 5 tagged studies.