Christiane E. Koch

ORCID: 0000-0003-4705-5669
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About
Contact & Profiles
Research Areas
  • Circadian rhythm and melatonin
  • Adipose Tissue and Metabolism
  • Regulation of Appetite and Obesity
  • Adipokines, Inflammation, and Metabolic Diseases
  • Dietary Effects on Health
  • Biochemical Analysis and Sensing Techniques
  • Sleep and Wakefulness Research
  • Stress Responses and Cortisol
  • Immune Response and Inflammation
  • Antibiotic Use and Resistance
  • Pancreatic function and diabetes
  • Photoreceptor and optogenetics research
  • Spaceflight effects on biology
  • Antibiotics Pharmacokinetics and Efficacy
  • Immune Cell Function and Interaction
  • Antibiotic Resistance in Bacteria
  • Tryptophan and brain disorders
  • Gestational Diabetes Research and Management
  • Genetics, Aging, and Longevity in Model Organisms
  • Greenhouse Technology and Climate Control
  • Retinal Imaging and Analysis
  • Neurogenetic and Muscular Disorders Research
  • Pregnancy and preeclampsia studies
  • Microgrid Control and Optimization
  • Peroxisome Proliferator-Activated Receptors

University Hospital Regensburg
2024

University of Lübeck
2014-2023

Institute of Neurobiology
2020

Innsbruck Medical University
2019

Philipps University of Marburg
2010-2018

University of Rostock
2012

High–fat (HF) diet-induced obesity and insulin insensitivity are associated with inflammation, particularly in white adipose tissue (WAT). However, is apparent within days of HF feeding when gains adiposity changes markers inflammation relatively minor. To investigate further the effects diet, C57Bl/6J mice were fed either a low (LF) or diet for 3 to 16 weeks, HF-diet matched caloric intake LF (PF) 1 week, time course glucose tolerance inflammatory gene expression measured liver, muscle WAT....

10.1371/journal.pone.0106159 article EN cc-by PLoS ONE 2014-08-29

Obesity is associated with resistance to the actions of both leptin and insulin via mechanisms that remain incompletely understood. To investigate whether per se contributes impaired glucose homeostasis, we investigated effect acute administration on homeostasis in normal as well leptin- or receptor-deficient mice. In hyperglycemic, leptin-deficient Lep ob/ob mice, acutely potently improved metabolism, before any change body fat mass, a mechanism involving p110α β isoforms...

10.1523/jneurosci.3202-10.2010 article EN cc-by-nc-sa Journal of Neuroscience 2010-12-01

Metabolic inflammation in the central nervous system might be causative for development of overnutrition-induced metabolic syndrome and related disorders, such as obesity, leptin insulin resistance, type 2 diabetes. Here we investigated whether nutritive genetic inhibition IκB kinase β (IKKβ)/nuclear factor-κB (NF-κB) pathway diet-induced obese (DIO) leptin-deficient mice improves these impairments. A known prominent inhibitor IKKβ/NF-κB signaling is dietary flavonoid butein. We initially...

10.2337/db14-0093 article EN Diabetes 2015-01-27

The occurrence of type II diabetes is highly correlated with obesity, although the mechanisms linking two conditions are incompletely understood. Leptin a potent insulin sensitiser and, in leptin-deficient, insensitive, Lep(ob/ob) mice, leptin improves glucose tolerance, indicating that resistance may link obesity to insensitivity. occurs response high-fat diet (HFD) and both hyperleptinaemia inflammation have been proposed as causative mechanisms. Scrutinising role this process, central...

10.1111/jne.12131 article EN Journal of Neuroendocrinology 2013-12-30

Circadian clocks coordinate 24-hr rhythms of behavior and physiology. In mammals, a master clock residing in the suprachiasmatic nucleus (SCN) is reset by light–dark cycle, while timed food intake potent synchronizer peripheral such as liver. Alterations can uncouple from SCN, resulting internal desynchrony, which promotes obesity metabolic disorders. Pancreas-derived hormones insulin glucagon have been implicated signaling mealtime to clocks. this study, we identify novel, more direct...

10.7554/elife.06253 article EN cc-by eLife 2015-03-30

Mutations in mitochondrial DNA (mtDNA) cause a variety of pathologic phenotypes. In this study, we used conplastic mouse strains to characterize the impact mtDNA mutation Atp8 gene on β-cell function, reactive oxygen species (ROS) generation, mass, and glucose metabolism response high-fat diet (HFD). comparison with B6-mtAKR controls, B6-mtFVB strain carries point mtDNA-coded (ATP synthase), leading fragmentated phenotype. Isolated pancreatic islets from 3-month-old mice showed increased...

10.1210/en.2012-1296 article EN Endocrinology 2012-09-21

GSK3β (glycogen synthase kinase 3β) is a ubiquitous that plays key role in multiple intracellular signalling pathways, and increased activity implicated disorders ranging from cancer to Alzheimer's disease. In the present study, we provide first evidence of hypothalamic via leptin-deficient Lep(ob/ob) mice show intracerebroventricular injection inhibitor acutely improves glucose tolerance these mice. The beneficial effect was dependent on PI3K (phosphoinositide 3-kinase), mediator both...

10.1042/bj20120834 article EN Biochemical Journal 2012-08-01

Abstract Unlimited access to calorie-dense, palatable food is a hallmark of Western societies and substantially contributes the worldwide rise metabolic disorders. In addition promoting overconsumption, diets dampen daily intake patterns, further augmenting disruption. We developed paradigm reveal differential timing in regulation behavior mice. While homeostatic peaks active phase, conditioned place preference choice experiments show an increased sensitivity overeating on during rest phase....

10.1038/s41467-020-16882-6 article EN cc-by Nature Communications 2020-06-17

Energy homeostasis is regulated by the hypothalamus but fails when animals are fed a high-fat diet (HFD), and leptin insensitivity obesity develops. To elucidate possible mechanisms underlying these effects, microarray-based transcriptomics approach was used to identify novel genes HFD in mouse hypothalamus.Mouse global array data identified serpinA3N as gene highly upregulated both challenge. In situ hybridisation showed expression upregulation all major hypothalamic nuclei agreement with...

10.1186/s12263-018-0619-1 article EN cc-by Genes & Nutrition 2018-11-29

Adiponectin, an adipocyte-derived hormone, regulates glucose and lipid metabolism. It is also antiinflammatory. During obesity, adiponectin levels sensitivity are reduced. Whereas the action of in periphery well established neuroendocrine role largely unknown. To address this we analyzed expression 2 receptors (AdipoR1 AdipoR2) response to fasting diet-induced genetic obesity. We investigated acute impact on central regulation homeostasis. Adiponectin (1 μg) was injected...

10.1210/en.2013-1734 article EN Endocrinology 2014-02-24

Endogenous circadian clocks have evolved to anticipate 24 hr rhythms in environmental demands. Recent studies suggest that rhythm disruption is a major risk factor for the development of metabolic disorders humans. Conversely, alterations energy state can disrupt behavior and physiology, creating vicious circle dysfunction. How peripheral affects diurnal food intake, however, still poorly understood. We here show adipokine adiponectin (ADIPOQ) regulates feeding through regulatory centers...

10.7554/elife.55388 article EN cc-by eLife 2020-07-09

Secondary metabolites of herbs and spices are widely used as an alternative strategy in the therapy various diseases. The polyphenols naringenin, quercetin curcumin have been characterised anti-diabetic agents. Conversely, vitro, naringenin described to inhibit phosphoinositide-3-kinase (PI3K), enzyme that is essential for neuronal control whole body glucose homoeostasis. Using both vitro vivo experiments, we tested whether inhibitory effect on PI3K occurs neurons if it might affect...

10.1017/s0007114512003005 article EN British Journal Of Nutrition 2012-08-01

In modern societies, the risk of developing a whole array affective and somatic disorders is associated with prevalence frequent psychosocial stress. Therefore, better understanding adaptive stress responses their underlying molecular mechanisms high clinical interest. response to an acute stressor, each organism can either show passive freezing or active fight-or-flight behaviour, activation sympathetic nervous system hypothalamus-pituitary-adrenal (HPA) axis providing necessary energy for...

10.1530/joe-16-0163 article EN Journal of Endocrinology 2016-09-23

Physiology and behaviour are critically dependent on circadian regulation via a core set of clock genes, dysregulation which leads to metabolic sleep disturbances. Metabolic perturbations occur in spinal muscular atrophy (SMA), neuromuscular disorder caused by loss the survival motor neuron (SMN) protein characterized muscle atrophy. We therefore investigated expression rhythm genes various tissues cord Taiwanese Smn-/-;SMN2 SMA animal model. demonstrate dysregulated (clock, ARNTL/Bmal1,...

10.1093/hmg/ddy249 article EN cc-by Human Molecular Genetics 2018-07-04

Abstract: Endogenous circadian timekeepers are found in most cells and organs of the body, including different types adipose tissues. This clock network orchestrates 24-hour rhythms physiology behavior to adapt organism daily recurring changes environment. Energy intake expenditure as well under control and, therefore, energy homeostasis function closely linked. In this review, we summarize current knowledge about regulation targets adipocyte clocks how rhythm disruption affects tissue...

10.2147/cpt.s116242 article EN ChronoPhysiology and Therapy 2017-04-01

Snacking, i.e., the intake of small amounts palatable food items, is a common behavior in modern societies, promoting overeating and obesity. Shifting into daily rest phase disrupts circadian rhythms also known to stimulate weight gain. We therefore hypothesized that chronic snacking inactive may promote body gain this effect based on disruption clocks.Male mice were fed chocolate snack either during their or active development metabolic parameters investigated. Snacking experiments repeated...

10.1016/j.molmet.2023.101691 article EN cc-by Molecular Metabolism 2023-02-04

Maternal and environmental factors control the epigenetic fetal programming of embryo, thereby defining susceptibility for metabolic or endocrine disorders in offspring. Pharmacological interventions required as a consequence gestational problems, e.g. hypertension, can potentially interfere with correct programming. As alterations are usually only revealed later life not detected studies focusing on early perinatal outcomes, little is known about long-term effects drug treatments. We sought...

10.1016/j.molmet.2017.06.016 article EN cc-by-nc-nd Molecular Metabolism 2017-07-01

Sleep is known to improve immune function ranging from cell distribution in the naïve state elevated antibody titers after an challenge. The underlying mechanisms still remain unclear, partially because most studies have focused on analysis of blood only. Hence, we investigated effects sleep within spleen female C57BL/6J mice with normal compared short-term sleep-deprived animals both and antigen Lack decreased expression genes associated recruitment into presentation during a T dependent B...

10.1016/j.bbih.2020.100082 article EN cc-by-nc-nd Brain Behavior & Immunity - Health 2020-05-01

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10.1017/s0029665111004551 article EN Proceedings of The Nutrition Society 2011-01-01
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