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Article: Muttermilch: Signalsystem der Evolution. Bodo C. Melnik hat zu den Wirkmechanismen des Enzymkomplexes mTORC1 im Zusammenhang mit dem Milchkonsum geforscht

Melnik, Bodo C.

2014 Volume -, Issue 1, Page(s) 58

Language	German
Document type	Article
ZDB-ID	80218-9
ISSN	0012-026x
Database	Current Contents Medicine

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Article: Interview mit Prof. Dr. Bodo C. Melnik: "Den Cocktail Milch verstehen". Birgit Heimbach im Gespräch über die metabolische und immunologische Programmierung durch Milch

Melnik, Bodo C. / Heimbach, Birgit

Deutsche Hebammen-Zeitschrift

2014 Volume -, Issue 1, Page(s) 63

Language	German
Document type	Article
ZDB-ID	80218-9
ISSN	0012-026x
Database	Current Contents Medicine

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Article ; Online: Metformin attenuates mechanistic target of rapamycin complex 1/hypoxia-inducible factor-1α-driven glycolysis reducing keratinocyte and T helper 17 cell proliferation in hyperproliferative inflammatory skin diseases.

Melnik, Bodo C

The British journal of dermatology

2023 Volume 189, Issue 6, Page(s) 652–653

MeSH term(s)	Humans ; Mechanistic Target of Rapamycin Complex 1/pharmacology ; Metformin/pharmacology ; Hidradenitis Suppurativa ; Hypoxia-Inducible Factor 1, alpha Subunit/pharmacology ; Keratinocytes/drug effects ; Glycolysis ; Cell Proliferation/drug effects ; Anti-Inflammatory Agents/pharmacology
Chemical Substances	Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Metformin (9100L32L2N) ; Hypoxia-Inducible Factor 1, alpha Subunit ; Anti-Inflammatory Agents
Language	English
Publishing date	2023-11-04
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	80076-4
ISSN	1365-2133 ; 0007-0963
ISSN (online)	1365-2133
ISSN	0007-0963
DOI	10.1093/bjd/ljad362
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Acne Transcriptomics: Fundamentals of Acne Pathogenesis and Isotretinoin Treatment.

Melnik, Bodo C

Cells

2023 Volume 12, Issue 22

Abstract: This review on acne transcriptomics allows for deeper insights into the pathogenesis of acne and isotretinoin's mode of action. Puberty-induced insulin-like growth factor 1 (IGF-1), insulin and androgen signaling activate the kinase AKT and mechanistic ... ...

Abstract	This review on acne transcriptomics allows for deeper insights into the pathogenesis of acne and isotretinoin's mode of action. Puberty-induced insulin-like growth factor 1 (IGF-1), insulin and androgen signaling activate the kinase AKT and mechanistic target of rapamycin complex 1 (mTORC1). A Western diet (hyperglycemic carbohydrates and milk/dairy products) also co-stimulates AKT/mTORC1 signaling. The AKT-mediated phosphorylation of nuclear FoxO1 and FoxO3 results in their extrusion into the cytoplasm, a critical switch which enhances the transactivation of lipogenic and proinflammatory transcription factors, including androgen receptor (AR), sterol regulatory element-binding transcription factor 1 (SREBF1), peroxisome proliferator-activated receptor γ (PPARγ) and signal transducer and activator of transcription 3 (STAT3), but reduces the FoxO1-dependent expression of GATA binding protein 6 (GATA6), the key transcription factor for infundibular keratinocyte homeostasis. The AKT-mediated phosphorylation of the p53-binding protein MDM2 promotes the degradation of p53. In contrast, isotretinoin enhances the expression of p53, FoxO1 and FoxO3 in the sebaceous glands of acne patients. The overexpression of these proapoptotic transcription factors explains isotretinoin's desirable sebum-suppressive effect via the induction of sebocyte apoptosis and the depletion of BLIMP1(+) sebocyte progenitor cells; it also explains its adverse effects, including teratogenicity (neural crest cell apoptosis), a reduced ovarian reserve (granulosa cell apoptosis), the risk of depression (the apoptosis of hypothalamic neurons), VLDL hyperlipidemia, intracranial hypertension and dry skin.
MeSH term(s)	Humans ; Isotretinoin/pharmacology ; Isotretinoin/therapeutic use ; Isotretinoin/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Tumor Suppressor Protein p53/metabolism ; Transcriptome/genetics ; Acne Vulgaris/drug therapy ; Acne Vulgaris/genetics ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Transcription Factors/metabolism
Chemical Substances	Isotretinoin (EH28UP18IF) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Tumor Suppressor Protein p53 ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Transcription Factors
Language	English
Publishing date	2023-11-10
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12222600
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Synergistic Effects of Milk-Derived Exosomes and Galactose on

Melnik, Bodo C

International journal of molecular sciences

2021 Volume 22, Issue 3

Abstract: Epidemiological studies associate milk consumption with an increased risk of Parkinson's disease (PD) and type 2 diabetes mellitus (T2D). PD is ... ...

Abstract	Epidemiological studies associate milk consumption with an increased risk of Parkinson's disease (PD) and type 2 diabetes mellitus (T2D). PD is an
MeSH term(s)	Animals ; Autophagy ; Biological Transport ; Cells, Cultured ; Diabetes Mellitus, Type 2/etiology ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/pathology ; Exosomes/metabolism ; Galactose/metabolism ; Galactose/pharmacology ; Humans ; Lysosomes/metabolism ; MicroRNAs/genetics ; Milk/metabolism ; Oxidative Stress ; Parkinson Disease/etiology ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Signal Transduction ; alpha-Synuclein/adverse effects ; alpha-Synuclein/metabolism
Chemical Substances	MicroRNAs ; alpha-Synuclein ; Galactose (X2RN3Q8DNE)
Language	English
Publishing date	2021-01-21
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22031059
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Dairy consumption and hepatocellular carcinoma risk.

Melnik, Bodo C

Annals of translational medicine

2021 Volume 9, Issue 8, Page(s) 736

Abstract: ... a hallmark of HCC promoted by hepatitis B virus (HBV) and hepatitis C virus (HCV). mTORC1 is also activated ...

Abstract	This review provides epidemiological and translational evidence for milk and dairy intake as critical risk factors in the pathogenesis of hepatocellular carcinoma (HCC). Large epidemiological studies in the United States and Europe identified total dairy, milk and butter intake with the exception of yogurt as independent risk factors of HCC. Enhanced activity of mechanistic target of rapamycin complex 1 (mTORC1) is a hallmark of HCC promoted by hepatitis B virus (HBV) and hepatitis C virus (HCV). mTORC1 is also activated by milk protein-induced synthesis of hepatic insulin-like growth factor 1 (IGF-1) and branched-chain amino acids (BCAAs), abundant constituents of milk proteins. Over the last decades, annual milk protein-derived BCAA intake increased 3 to 5 times in Western countries. In synergy with HBV- and HCV-induced secretion of hepatocyte-derived exosomes enriched in microRNA-21 (miR-21) and miR-155, exosomes of pasteurized milk as well deliver these oncogenic miRs to the human liver. Thus, milk exosomes operate in a comparable fashion to HBV- or HCV- induced exosomes. Milk-derived miRs synergistically enhance IGF-1-AKT-mTORC1 signaling and promote mTORC1-dependent translation, a meaningful mechanism during the postnatal growth phase, but a long-term adverse effect promoting the development of HCC. Both, dietary BCAA abundance combined with oncogenic milk exosome exposure persistently overstimulate hepatic mTORC1. Chronic alcohol consumption as well as type 2 diabetes mellitus (T2DM), two HCC-related conditions, increase BCAA plasma levels. In HCC, mTORC1 is further hyperactivated due to
Language	English
Publishing date	2021-04-16
Publishing country	China
Document type	Journal Article ; Review
ZDB-ID	2893931-1
ISSN	2305-5847 ; 2305-5839
ISSN (online)	2305-5847
ISSN	2305-5839
DOI	10.21037/atm-2020-ubih-06
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Lifetime Impact of Cow's Milk on Overactivation of mTORC1: From Fetal to Childhood Overgrowth, Acne, Diabetes, Cancers, and Neurodegeneration.

Melnik, Bodo C

Biomolecules

2021 Volume 11, Issue 3

Abstract: The consumption of cow's milk is a part of the basic nutritional habits of Western industrialized countries. Recent epidemiological studies associate the intake of cow's milk with an increased risk of diseases, which are associated with overactivated ... ...

Abstract	The consumption of cow's milk is a part of the basic nutritional habits of Western industrialized countries. Recent epidemiological studies associate the intake of cow's milk with an increased risk of diseases, which are associated with overactivated mechanistic target of rapamycin complex 1 (mTORC1) signaling. This review presents current epidemiological and translational evidence linking milk consumption to the regulation of mTORC1, the master-switch for eukaryotic cell growth. Epidemiological studies confirm a correlation between cow's milk consumption and birthweight, body mass index, onset of menarche, linear growth during childhood, acne vulgaris, type 2 diabetes mellitus, prostate cancer, breast cancer, hepatocellular carcinoma, diffuse large B-cell lymphoma, neurodegenerative diseases, and all-cause mortality. Thus, long-term persistent consumption of cow's milk increases the risk of mTORC1-driven diseases of civilization. Milk is a highly conserved, lactation genome-controlled signaling system that functions as a maternal-neonatal relay for optimized species-specific activation of mTORC1, the nexus for regulation of eukaryotic cell growth, and control of autophagy. A deeper understanding of milk´s impact on mTORC1 signaling is of critical importance for the prevention of common diseases of civilization.
MeSH term(s)	Acne Vulgaris/pathology ; Animals ; Cattle ; Child ; Child Development ; Diabetes Mellitus/pathology ; Fetus/pathology ; Humans ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Milk/adverse effects ; Neoplasms/pathology ; Nerve Degeneration/pathology
Chemical Substances	Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2021-03-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom11030404
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Milk exosomal miRNAs: potential drivers of AMPK-to-mTORC1 switching in β-cell de-differentiation of type 2 diabetes mellitus.

Melnik, Bodo C

Nutrition & metabolism

2019 Volume 16, Page(s) 85

Abstract: Type 2 diabetes mellitus (T2DM) steadily increases in prevalence since the 1950's, the period of widespread distribution of refrigerated pasteurized cow's milk. Whereas breastfeeding protects against the development of T2DM in later life, accumulating ... ...

Abstract	Type 2 diabetes mellitus (T2DM) steadily increases in prevalence since the 1950's, the period of widespread distribution of refrigerated pasteurized cow's milk. Whereas breastfeeding protects against the development of T2DM in later life, accumulating epidemiological evidence underlines the role of cow's milk consumption in T2DM. Recent studies in rodent models demonstrate that during the breastfeeding period pancreatic
Language	English
Publishing date	2019-12-06
Publishing country	England
Document type	Journal Article
ZDB-ID	2160376-5
ISSN	1743-7075
ISSN	1743-7075
DOI	10.1186/s12986-019-0412-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Milk Exosomal microRNAs: Postnatal Promoters of β Cell Proliferation but Potential Inducers of β Cell De-Differentiation in Adult Life.

Melnik, Bodo C / Schmitz, Gerd

International journal of molecular sciences

2022 Volume 23, Issue 19

Abstract: ... to bovine MEX. Mechanistic evidence suggests that MEX miRs stimulate mTORC1/c-MYC-dependent postnatal β ...

Abstract	Pancreatic β cell expansion and functional maturation during the birth-to-weaning period is driven by epigenetic programs primarily triggered by growth factors, hormones, and nutrients provided by human milk. As shown recently, exosomes derived from various origins interact with β cells. This review elucidates the potential role of milk-derived exosomes (MEX) and their microRNAs (miRs) on pancreatic β cell programming during the postnatal period of lactation as well as during continuous cow milk exposure of adult humans to bovine MEX. Mechanistic evidence suggests that MEX miRs stimulate mTORC1/c-MYC-dependent postnatal β cell proliferation and glycolysis, but attenuate β cell differentiation, mitochondrial function, and insulin synthesis and secretion. MEX miR content is negatively affected by maternal obesity, gestational diabetes, psychological stress, caesarean delivery, and is completely absent in infant formula. Weaning-related disappearance of MEX miRs may be the critical event switching β cells from proliferation to TGF-β/AMPK-mediated cell differentiation, whereas continued exposure of adult humans to bovine MEX miRs via intake of pasteurized cow milk may reverse β cell differentiation, promoting β cell de-differentiation. Whereas MEX miR signaling supports postnatal β cell proliferation (diabetes prevention), persistent bovine MEX exposure after the lactation period may de-differentiate β cells back to the postnatal phenotype (diabetes induction).
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Adult ; Animals ; Cattle ; Cell Differentiation ; Cell Proliferation ; Exosomes/metabolism ; Female ; Humans ; Infant ; Insulin/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Milk/metabolism ; Milk, Human/metabolism ; Pregnancy ; Transforming Growth Factor beta/metabolism
Chemical Substances	Insulin ; MicroRNAs ; Transforming Growth Factor beta ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2022-09-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms231911503
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Synergistic Effects of Milk-Derived Exosomes and Galactose on α -Synuclein Pathology in Parkinson’s Disease and Type 2 Diabetes Mellitus

Bodo C. Melnik

International Journal of Molecular Sciences, Vol 22, Iss 3, p

2021 Volume 1059

Abstract: ... activate c-Abl-mediated aggregation of α -syn which is exported by exosome release. Via the vagal nerve and ...

Abstract	Epidemiological studies associate milk consumption with an increased risk of Parkinson’s disease (PD) and type 2 diabetes mellitus (T2D). PD is an α -synucleinopathy associated with mitochondrial dysfunction, oxidative stress, deficient lysosomal clearance of α -synuclein ( α -syn) and aggregation of misfolded α -syn. In T2D, α -syn promotes co-aggregation with islet amyloid polypeptide in pancreatic β -cells. Prion-like vagal nerve-mediated propagation of exosomal α -syn from the gut to the brain and pancreatic islets apparently link both pathologies. Exosomes are critical transmitters of α -syn from cell to cell especially under conditions of compromised autophagy. This review provides translational evidence that milk exosomes (MEX) disturb α -syn homeostasis. MEX are taken up by intestinal epithelial cells and accumulate in the brain after oral administration to mice. The potential uptake of MEX miRNA-148a and miRNA-21 by enteroendocrine cells in the gut, dopaminergic neurons in substantia nigra and pancreatic β -cells may enhance miRNA-148a/DNMT1-dependent overexpression of α -syn and impair miRNA-148a/PPARGC1A- and miRNA-21/LAMP2A-dependent autophagy driving both diseases. MiRNA-148a- and galactose-induced mitochondrial oxidative stress activate c-Abl-mediated aggregation of α -syn which is exported by exosome release. Via the vagal nerve and/or systemic exosomes, toxic α -syn may spread to dopaminergic neurons and pancreatic β -cells linking the pathogenesis of PD and T2D.
Keywords	autophagy ; DNA methyltransferase 1 ; diabetes mellitus ; galactose ; milk exosome ; milk microRNAs ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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