Holger Henneicke

ORCID: 0000-0003-1746-9369
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About
Contact & Profiles
Research Areas
  • Adrenal Hormones and Disorders
  • Stress Responses and Cortisol
  • Bone Metabolism and Diseases
  • Adipose Tissue and Metabolism
  • Bone health and osteoporosis research
  • Estrogen and related hormone effects
  • Vitamin D Research Studies
  • Hormonal Regulation and Hypertension
  • Adipokines, Inflammation, and Metabolic Diseases
  • Cytokine Signaling Pathways and Interactions
  • Hormonal and reproductive studies
  • Osteoarthritis Treatment and Mechanisms
  • COVID-19 Clinical Research Studies
  • Eicosanoids and Hypertension Pharmacology
  • Growth Hormone and Insulin-like Growth Factors
  • Biomarkers in Disease Mechanisms
  • Bone health and treatments
  • Prostate Cancer Treatment and Research
  • Diet and metabolism studies
  • Exercise and Physiological Responses
  • Pituitary Gland Disorders and Treatments
  • Knee injuries and reconstruction techniques
  • Regulation of Appetite and Obesity
  • Inflammatory mediators and NSAID effects
  • Cancer, Stress, Anesthesia, and Immune Response

Technische Universität Dresden
2016-2023

University Hospital Carl Gustav Carus
2020-2023

Anzac Research Institute
2008-2021

The University of Sydney
2009-2021

Deutsche Forschungsgemeinschaft
2016

German Rheumatism Research Centre
2012

Charité - Universitätsmedizin Berlin
2008-2012

Sydney Hospital
2008

Long-term glucocorticoid treatment is associated with numerous adverse outcomes, including weight gain, insulin resistance, and diabetes; however, the pathogenesis of these side effects remains obscure. Glucocorticoids also suppress osteoblast function, osteocalcin synthesis. Osteocalcin an osteoblast-specific peptide that reported to be involved in normal murine fuel metabolism. We now demonstrate osteoblasts play a pivotal role glucocorticoid-induced dysmetabolism. Osteoblast-targeted...

10.1172/jci63377 article EN Journal of Clinical Investigation 2012-10-24

Abstract Chronic high-fat diet (HFD) consumption not only promotes obesity and insulin resistance, but also causes bone loss through mechanisms that are well understood. Here, we fed wild-type CD-1 mice either chow or a HFD (43% of energy from fat) for 18 weeks; HFD-fed exhibited decreased trabecular volume (−28%) cortical thickness (−14%) compared to chow-fed mice. In mice, was due reduced formation mineral apposition, without obvious effects on resorption. feeding increased skeletal...

10.1038/s41413-021-00159-9 article EN cc-by Bone Research 2021-09-01

The hypothalamus-pituitary-adrenal (HPA) axis is activated in response to inflammation leading increased production of anti-inflammatory glucocorticoids by the adrenal cortex, thereby representing an endogenous feedback loop. However, severe reduces responsiveness gland adrenocorticotropic hormone (ACTH), although underlying mechanisms are poorly understood. Here, we show transcriptomic, proteomic, and metabolomic analyses that LPS-induced systemic triggers profound metabolic changes...

10.7554/elife.83064 article EN cc-by eLife 2023-07-14

Mutations in PIK3CA, the gene encoding p110α catalytic subunit of PI3K, are among most common mutations found human cancer and have also recently been implicated a range overgrowth syndromes humans. We used novel inducible "exonswitch" approach to knock constitutively active Pik3caH1047R mutation into endogenous Pik3ca mouse. Ubiquitous expression throughout body resulted dramatic increase weight within 3 weeks induction (mutant 150 ± 5%; wild-type 117 3%, mean sem), which was associated...

10.1096/fj.14-262782 article EN The FASEB Journal 2014-12-30

Abstract Chronic stress and depression are associated with alterations in the hypothalamic–pituitary–adrenal signaling cascade considered a risk factor for bone loss fractures. However, mechanisms underlying association between poor health unclear. Using transgenic (tg) mouse model which glucocorticoid is selectively disrupted mature osteoblasts osteocytes [11β-hydroxysteroid-dehydrogenase type 2 (HSD2)OB-tg mice], present study examines impact of chronic on skeletal metabolism structure....

10.1210/en.2016-1658 article EN Endocrinology 2017-03-22

Elevated serum concentrations of glucocorticoids (GCs) result in excessive lipid accumulation white adipose tissue (WAT) as well dysfunction thermogenic brown (BAT), ultimately leading to the development obesity and metabolic disease. Here, we hypothesized that activation sympathetic nervous system either via cold exposure or use a selective β3-adrenergic receptor (β3-AR) agonist alleviates adverse effects chronic GC rodents. To this end, male 10-wk-old C57BL/6NRj mice were treated with...

10.1152/ajpendo.00259.2022 article EN AJP Endocrinology and Metabolism 2023-04-26

Aging and chronic glucocorticoid excess share a number of critical features, including the development central obesity, insulin resistance osteoporosis. Previous studies have shown that skeletal signalling increases with aging osteoblasts mediate detrimental metabolic effects excess. Here, we investigated whether endogenous action in skeleton contributes to dysfunction during normal aging. Mice lacking osteocytes (HSD2OB/OCY-tg mice) their wild-type littermates were studied until 3, 6, 12 18...

10.1016/j.molmet.2020.101098 article EN cc-by-nc-nd Molecular Metabolism 2020-10-10

Abstract BACKGROUND Glucocorticoids influence prostate development and pathology, yet the underlying mechanisms including possible direct glucocorticoid effect on are not well characterized. METHODS We evaluated expression of receptor (GR) together with effects supraphysiological (corticosterone) mouse morphology epithelial proliferation. Mature male mice were treated by weekly subdermal implantation depot pellets containing either 1.5 mg corticosterone or placebo providing steady‐state...

10.1002/pros.21242 article EN The Prostate 2010-08-17
Stefan R. Bornstein Kaomei Guan Coy Brunßen Gregor Mueller Virginia Kamvissi-Lorenz and 89 more Robert I. Lechler Richard C. Trembath Manuel Mayr Lucilla Poston Rocı́o Sancho S. Ahmed Ezz Al-Din Ahmed Al-Far Bassam Aljani Tiago C. Alves Stephanie A. Amiel Cynthia L. Andoniadou Manjunath Reddy Bandral Alexia Belavgeni Ilona Berger Andreas L. Birkenfeld Ezio Bonifacio Triantafyllos Chavakis P. Chawla Pratik Choudhary Ana-Maria Cujba Luis Fernando Delgadillo-Silva Theoni Ingrid Demcollari Denise M. Drotar Sarah Duin Nermeen N. El-Agroudy Ali El‐Armouche Anne Eugster Manuel Gado Anthony Gavalas Michael Gelinsky M. Guirgus Sinah Hansen Emily Hanton M. Hasse Holger Henneicke Carolin Heller H C Hempel Christer Högstrand David Hopkins L. Jarc Peter M. Jones Margrit Kamel Susanne Kämmerer Aileen King Anica Kurzbach Christian Lambert Y. Latunde-Dada Ivo Lieberam Josephine Liers J. W. Li Andreas Linkermann Sophie Locke Barbara Ludwig Teodora Manea Francesca Maremonti Zuzana Mariničová Barbara McGowan Marius Mickunas Geltrude Mingrone Karthikeyan Mohanraj Henning Morawietz Nikolay Ninov Mark Peakman Shanta J. Persaud Jens Pietzsch Eleder Cachorro Timothy J. Pullen Iryna Pyrina Francesco Rubino Alice Santambrogio Florian Schepp Pia Schlinkert Laura D. Scriba Richard Siow Michele Solimena Francesca M. Spagnoli Stephan Speier Androniki Stavridou Charlotte Steenblock Anna Strano Paul Taylor A. Tiepner Wulf Tonnus Timothy Tree Fiona M. Watt Martin Werdermann Michael Wilson Nasrullah Yusuf Christian G. Ziegler

Currently, we are experiencing a true pandemic of communicable disease by the virus SARS-CoV-2 holding whole world firmly in its grasp. Amazingly and unfortunately, this uses metabolic endocrine pathway via ACE2 to enter our cells causing damage disease. Our international research training programme funded German Research Foundation has clear mission train best students wherever they may come from learn tackle enormous challenges diabetes complications for society. A modern metabolism does...

10.1055/a-1377-6583 article EN Hormone and Metabolic Research 2021-03-01

Searchable abstracts of presentations at key conferences on calcified tissues ISSN 2052-1219 (online)

10.1530/boneabs.5.p491 article EN Bone Abstracts 2016-04-21

Searchable abstracts of presentations at key conferences on calcified tissues ISSN 2052-1219 (online)

10.1530/boneabs.5.ni7 article EN Bone Abstracts 2016-04-21

Despite their desired immunosuppressive properties, glucocorticoids (GCs) are associated with multiple adverse effects severely limiting clinical use. Patients receiving continuous GC therapy frequently suffer from a reduced bone mass and high propensity for spinal fractures, rendering glucocorticoid-induced osteoporosis (GIO) the most common form of secondary osteoporosis. The sympathetic nervous system has been shown to be potent regulator metabolism. Here we examine possible interaction...

10.1055/s-0039-1680042 article EN Osteologie/Osteology 2019-02-01

Abstract The hypothalamus-pituitary-adrenal (HPA) axis is activated in response to inflammation leading increased production of anti-inflammatory glucocorticoids by the adrenal cortex, thereby representing an endogenous feedback loop. However, severe reduces responsiveness gland adrenocorticotropic hormone (ACTH) although underlying mechanisms are poorly understood. Here, we show transcriptomic, proteomic and metabolomic analyses that LPS-induced systemic triggers profound metabolic changes...

10.1101/2022.04.29.490066 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2022-05-01
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