Jerome Nicolas Marius Ruzzin

Pregnane X receptor deletion induces a lean phenotype in chow-fed mice through a liver-ileum-muscle axis involving 6α-hydroxylated bile acids and Fgf15. Mol Metab 2026 Impact Factor: 6.6

Transcriptomic profiling of co-cultured cancer-host cells identifies hypoxia as a driver of the skeletal muscle cell's anti-proliferative effect on cancer cells. Oncogenesis 2026. Impact Factor: 6.4

Therapeutic potential of FGF19 in combatting osteosarcopenia: effects on muscle strength and bone health in aged male mice. JMBR Plus 2025. Impact Factor: 3.8

Persistent organic pollutants disrupt the oxidant/antioxidant balance of INS-1E pancreatic β-cells causing their physiological dysfunctions. Environment International 2024 . Impact Factor: 11.8

Mice lacking intestinal Nr1i2 have normal intestinal homeostasis under steady-state conditions and are not hypersensitive to inflammation under lipopolysaccharide treatment. FASEB Journal 2023 - Impact Factor: 5.83

Associations between persistent organic pollutants and type 1 diabetes in youth. Environment International 2022 . Impact Factor: 13.35

Treatment with fibroblast growth factor 19 increases skeletal muscle fiber size, ameliorates metabolic perturbations and hepatic inflammation in 5/6 nephrectomized mice. Science Reports 2023 - Impact factor: 4.99 

Fibroblast growth factor 19 as a countermeasure to muscle and locomotion dysfunctions in experimental cerebral palsy. Journal of Cachexia, Sarcopenia and Muscle 2021 - Impact Factor: 12.91

Fibroblast growth factor 19 regulates skeletal muscle mass and protects from muscle wasting. Nature Medicine 2017 - Impact Factor: 32.62

Environmental Health Perspectives (2010), PLoS ONE (2011), Journal of Clinical Endocrinology & Metabolism (2014). 

• Aunan, Anine; Claeyssen, Charlotte; Abdelhalim, Mohamed & Ruzzin, Jerome Nicolas Marius (2026). Transcriptomic profiling of co-cultured cancer-host cells identifies hypoxia as a driver of the skeletal muscle cell’s anti-proliferative effect on cancer cells | Oncogenesis. Oncogenesis. doi: 10.1038/s41389-026-00601-9. Full text in Research Archive Show summary

  Cancer metastasis is the leading cause of cancer-related death. While organs such as the lung are hotspots for metastases, others -like skeletal muscle- remain rarely colonized, a phenomenon that remains poorly understood. In this study, we show that EO771 breast cancer cells proliferated robustly when co-cultured with MLg lung stromal cells, whereas their proliferation was restrained when maintained in direct contact with differentiated C2C12 skeletal muscle myotubes. Notably, these effects were not cell-type-specific, as similar results were obtained with 4T1 breast cancer cells and Sol8 myotubes. After two days of co-culture, both cancer and host cells (MLg and C2C12) exhibited distinct niche-specific transcriptional remodeling. Strikingly, the poorly proliferative EO771 cells co-cultured with C2C12 myotubes acquired a hypoxia-associated gene-expression signature despite normoxic conditions (~20% O₂), showing that muscle cells reprogram cancer cells into a hypoxic, anti-proliferative state. Under hypoxic conditions, we confirmed that the depletion of oxygen allows C2C12 cells to nearly abolish EO771 proliferation. Neither exogenous lactate, culture acidosis, their combination, altered glucose levels, nor conditioned medium could reproduce the suppressive environment created by C2C12 myotubes. In contrast, MLg cells induced minimal transcriptional changes in EO771 cells and were themselves broadly reprogrammed by the cancer cells. Moreover, hypoxia enhanced EO771 proliferation in MLg co-cultures, emphasizing the permissive nature of the MLg environment. Collectively, these findings uncover a unique, paradoxical, muscle-induced pseudo-hypoxic program that restricts cancer cell proliferation. They also highlight the need for caution in targeting hypoxia signaling in anti-metastatic therapies, as such interventions could weaken skeletal muscle’s natural defense against tumor colonization.

• Bresson, Sophie Emilie & Ruzzin, Jerome Nicolas Marius (2024). Persistent organic pollutants disrupt the oxidant/antioxidant balance of INS-1E pancreatic β-cells causing their physiological dysfunctions. Environment International. ISSN 0160-4120. 190. doi: 10.1016/j.envint.2024.108821. Full text in Research Archive Show summary

  Background Persistent organic pollutants (POPs) have emerged as potent diabetogenic agents, but their mechanisms of action remain poorly identified. Objectives In this study, we aim to determine the mechanisms regulating the damaging effects of POPs in pancreatic β-cells, which have a central role in the development of diabetes. Methods We treated INS-1E pancreatic β-cells with PCB-153, p,p’-DDE, PCB-126, or TCDD at doses ranging from 1 × 10-15 to 5 × 10-6 M. We measured insulin content and secretion, cell viability and assessed the mRNA expression of the xenobiotic nuclear receptors Nr1i2 and Nr1i3, and the aryl hydrocarbon receptor (Ahr). In addition, we evaluated the antioxidant defense and production of reactive oxygen species (ROS). Finally, we studied the ability of the antioxidant N-acetyl-L-cysteine (NAC) to counteract the effects of POPs in INS-1E cells. Results When exposed to environmental POP levels, INS-1E cells had impaired production and secretion of insulin. These defects were observed for all tested POPs and were paralleled by reduced Ins1 and Ins2 mRNA expression. While POP treatment for 3 days did not affect INS-1E cell viability, longer treatment progressively killed the cells. Furthermore, we found that the xenobiotic detoxification machinery is poorly expressed in the INS-1E cells, as characterized by the absence of Nr1i2 and Nr1i3 and their respective downstream targets Cyp3a1/Cyp3a2 and Cyp2b1/Cyp2b3, and the weak functionality of the Ahr/Cyp1a1 signaling. Interestingly, POPs dysregulated key antioxidant enzymes such as glutathione peroxidases, peroxiredoxins, thioredoxins, and catalases. In parallel, the production of intracellular ROS, including superoxide anion (O2•−) and hydrogen peroxide (H2O2), was increased by POP exposure. Improving the oxidant scavenging capacity of INS-1E cells by NAC treatment restored the production and secretion of insulin. Conclusion By promoting oxidative stress and impairing the ability of INS-1E cells to produce and secrete insulin, this study reveals how POPs can mechanistically act as diabetogenic agents, and provides new scientific evidence supporting the concept that POPs are fueling the diabetes epidemics.

• Benoit, Berengère; Beau, Alice; Bres, Émilie; Chanon, Stéphanie; Pinteur, Claudie & Vieille-Marchiset, Aurélie [Show all 14 contributors for this article] (2023). Treatment with fibroblast growth factor 19 increases skeletal muscle fiber size, ameliorates metabolic perturbations and hepatic inflammation in 5/6 nephrectomized mice. Scientific Reports. 13. doi: 10.1038/s41598-023-31874-4. Full text in Research Archive Show summary

  Abstract Chronic kidney disease (CKD) is associated with osteosarcopenia, and because a physical decline in patients correlates with an increased risk of morbidity, an improvement of the musculoskeletal system is expected to improve morbi-mortality. We recently uncovered that the intestinal hormone Fibroblast Growth Factor 19 (FGF19) is able to promote skeletal muscle mass and strength in rodent models, in addition to its capacity to improve glucose homeostasis. Here, we tested the effects of a treatment with recombinant human FGF19 in a CKD mouse model, which associates sarcopenia and metabolic disorders. In 5/6 nephrectomized (5/6Nx) mice, subcutaneous FGF19 injection (0.1 mg/kg) during 18 days increased skeletal muscle fiber size independently of food intake and weight gain, associated with decreased gene expression of myostatin. Furthermore, FGF19 treatment attenuated glucose intolerance and reduced hepatic expression of gluconeogenic genes in uremic mice. Importantly, the treatment also decreased gene expression of liver inflammatory markers in CKD mice. Therefore, our results suggest that FGF19 may represent a novel interesting therapeutic strategy for a global improvement of sarcopenia and metabolic complications in CKD.

• Amini, Salah Edden; Bresson, Sophie Emilie & Ruzzin, Jerome Nicolas Marius (2023). Mice lacking intestinal Nr1i2 have normal intestinal homeostasis under steady-state conditions and are not hypersensitive to inflammation under lipopolysaccharide treatment. The FASEB Journal. ISSN 0892-6638. 37(8). doi: 10.1096/fj.202301126. Full text in Research Archive Show summary

  Abstract Nr1i2 , a nuclear receptor known for its key function in xenobiotic detoxification, has emerged as a potential regulator of intestinal homeostasis and inflammation. However, the role of Nr1i2 in different intestinal segments remains poorly known. Moreover, in vivo investigations on intestinal Nr1i2 have essentially been performed in whole‐body Nr1i2 knockout ( Nr1i2 −/− ) mice where the deletion of Nr1i2 in all tissues may affect the intestinal phenotype. To better understand the role of Nr1i2 in the intestine, we generated intestinal epithelial‐specific Nr1i2 knockout (i Nr1i2 −/− ) mice and studied the duodenum, jejunum, ileum, and colon of these animals during steady‐state conditions and lipopolysaccharide (LPS)‐induced inflammation. As compared to control (i Nr1i2 +/+ ) mice, i Nr1i2 −/− mice showed normal intestinal permeability as assessed by in vivo FITC‐dextran test. The expression of genes involved in inflammation, tight‐ and adherens‐junction, proliferation, glucose, and lipid metabolism was comparable in the duodenum, jejunum, ileum, and colon of i Nr1i2 −/− and i Nr1i2 +/+ mice. In line with these findings, histological analyses of the jejunum revealed no difference between i Nr1i2 −/− and i Nr1i2 +/+ mice. When treated with LPS, the intestine of i Nr1i2 −/− mice had no increased inflammatory response as compared to i Nr1i2 +/+ mice. Moreover, the health monitoring of LPS‐treated i Nr1i2 −/− and i Nr1i2 +/+ mice was similar. Taken together, our results demonstrate that the specific deletion of Nr1i2 in the intestinal epithelium does not cause major intestinal damages in mice during both steady‐state and inflammatory conditions.

• Bresson, Sophie Emilie; Isom, Scott; Jensen, ET; Huber, Sandra; Oulhote, Youssef & Rigdon, Joseph [Show all 12 contributors for this article] (2022). Associations between persistent organic pollutants and type 1 diabetes in youth. Environment International. ISSN 0160-4120. 163. doi: 10.1016/j.envint.2022.107175. Full text in Research Archive Show summary

  Background: Diabetes affects millions of people worldwide with a continued increase in incidence occurring within the pediatric population. The potential contribution of persistent organic pollutants (POPs) to diabetes in youth remains poorly known, especially regarding type 1 diabetes (T1D), generally the most prevalent form of diabetes in youth. Objectives: We investigated the associations between POPs and T1D in youth and studied the impacts of POPs on pancreatic β-cell function and viability in vitro. Methods: We used data and plasma samples from the SEARCH for Diabetes in Youth Case Control Study (SEARCH-CC). Participants were categorized as Controls, T1D with normal insulin sensitivity (T1D/IS), and T1D with insulin resistance (T1D/IR). We assessed plasma concentrations of polychlorinated biphenyls (PCBs) and organochlorine pesticides and estimated the odds of T1D through multivariable logistic regression. In addition, we performed in vitro experiments with the INS-1E pancreatic β-cells. Cells were treated with PCB-153 or p,p’- DDE at environmentally relevant doses. We measured insulin production and secretion and assessed the mRNA expression of key regulators involved in insulin synthesis (Ins1, Ins2, Pdx1, Mafa, Pcsk1/3, and Pcsk2), glucose sensing (Slc2a2 and Gck), and insulin secretion (Abcc8, Kcnj11, Cacna1d, Cacna1b, Stx1a, Snap25, and Sytl4). Finally, we assessed the effects of PCB-153 and p,p’-DDE on β-cell viability. Results: Among 442 youths, 112 were controls, 182 were classified with T1D/IS and 148 with T1D/IR. The odds ratios (OR) of T1D/IS versus controls were statistically significant for p,p’-DDE (OR 2.0, 95% confidence interval (CI) 1.0, 3.8 and 2.4, 95% CI 1.2, 5.0 for 2nd and 3rd tertiles, respectively), trans-nonachlor (OR 2.5, 95% CI 1.3, 5.0 and OR 2.3, 95% CI 1.1, 5.1 for 2nd and 3rd tertiles, respectively), and PCB-153 (OR 2.3, 95% CI 1.1, 4.6 for 3rd tertile). However, these associations were not observed in participants with T1D/IR. At an experimental level, treatment with p,p’-DDE or PCB-153, at concentrations ranging from 1 × 10-15 M to 5 × 10-6 M, impaired the ability of pancreatic β-cells to produce and secrete insulin in response to glucose. These failures were par- alleled by impaired Ins1 and Ins2 mRNA expression. In addition, among different targeted genes, PCB-153 significantly reduced Slc2a2 and Gck mRNA expression whereas p,p’-DDE mainly affected Abcc8 and Kcnj11. While treatment with PCB-153 or p,p’-DDE for 2 days did not affect β-cell viability, longer treatment progres- sively killed the β-cells

• Pereira, Sabrina da Conceição; Benoit, Bérengère; Junior, Francisco Carlos Amanajás de Aguiar; Chanon, Stéphanie; Vieille-Marchiset, Aurélie & Pesenti, Sandra [Show all 9 contributors for this article] (2021). Fibroblast growth factor 19 as a countermeasure to muscle and locomotion dysfunctions in experimental cerebral palsy. Journal of Cachexia, Sarcopenia and Muscle. ISSN 2190-5991. 12(6), p. 2122–2133. doi: 10.1002/jcsm.12819. Full text in Research Archive Show summary

  Background Cerebral palsy (CP) associates cerebral function damages with strong locomotor defects and premature sarcopenia. We previously showed that fibroblast growth factor 19 (FGF19) exerts hypertrophic effects on skeletal muscle and improves muscle mass and strength in mouse models with muscle atrophy. Facing the lack of therapeutics to treat locomotor dysfunctions in CP, we investigated whether FGF19 treatment could have beneficial effects in an experimental rat model of CP. Methods Cerebral palsy was induced in male Wistar rat pups by perinatal anoxia immediately after birth and by sensorimotor restriction of hind paws maintained until Day 28. Daily subcutaneous injections with recombinant human FGF19 (0.1 mg/kg bw) were performed from Days 22 to 28. Locomotor activity and muscle strength were assessed before and after FGF19 treatment. At Day 29, motor coordination on rotarod and various musculoskeletal parameters (weight of tibia bone and of soleus and extensor digitorum longus (EDL) muscles; area of skeletal muscle fibres) were evaluated. In addition, expression of specific genes linked to human CP was measured in rat skeletal muscles. Results Compared to controls, CP rats had reduced locomotion activity (−37.8% of distance travelled, P < 0.05), motor coordination (−88.9% latency of falls on rotarod, P < 0.05) and muscle strength (−25.1%, P < 0.05). These defects were associated with reduction in soleus (−51.5%, P < 0.05) and EDL (−42.5%, P < 0.05) weight, smaller area of muscle fibres, and with lower tibia weight (−38%, P < 0.05). In muscles from rats submitted to CP, changes in the expression levels of several genes related to muscle development and neuromuscular junctions were similar to those found in wrist muscle of children with CP (increased mRNA levels of Igfbp5, Kcnn3, Gdf8, and MyH4 and decreased expression of Myog, Ucp2 and Lpl). Compared with vehicle-treated CP rats, FGF19 administration improved locomotor activity (+53.2%, P < 0.05) and muscle strength (+25.7%, P < 0.05), and increased tibia weight (+13.8%, P < 0.05) and soleus and EDL muscle weight (+28.6% and +27.3%, respectively, P < 0.05). In addition, it reduced a number of very small fibres in both muscles (P < 0.05). Finally, gene expression analyses revealed that FGF19 might counteract the immature state of skeletal muscles induced by CP. Conclusions These results demonstrate that pharmacological intervention with recombinant FGF19 could restore musculoskeletal and locomotor dysfunction in an experimental CP model, suggesting that FGF19 may represent a potential therapeutic strategy to combat the locomotor disorders associated with CP.

• Dusanov, Sasa; Svendsen, Mette; Ruzzin, Jerome; Kiviranta, Hannu; Gulseth, Hanne Løvdal & Klemsdal, Tor Ole [Show all 7 contributors for this article] (2019). Effect of fatty fish or nut consumption on concentrations of persistent organic pollutants in overweight or obese men and women: A randomized controlled clinical trial. NMCD. Nutrition Metabolism and Cardiovascular Diseases. ISSN 0939-4753. 30(3), p. 448–458. doi: 10.1016/j.numecd.2019.11.006. Full text in Research Archive
• Dusanov, Sasa; Ruzzin, Jérôme; Kiviranta, Hannu; Klemsdal, Tor Ole; Retterstøl, Lars & Rantakokko, Panu [Show all 9 contributors for this article] (2018). Associations between persistent organic pollutants and metabolic syndrome in morbidly obese individuals. NMCD. Nutrition Metabolism and Cardiovascular Diseases. ISSN 0939-4753. p. 1–8. doi: 10.1016/j.numecd.2018.03.004. Full text in Research Archive
• Benoit, Berengère; Meugnier, Emmanuelle; Castelli, Martina Galatea; Chanon, Stéphanie; Vieille-Marchiset, Aurélie & Durand, Christine [Show all 15 contributors for this article] (2017). Fibroblast growth factor 19 regulates skeletal muscle mass and ameliorates muscle wasting in mice. Nature Medicine. ISSN 1078-8956. 23(8), p. 990–996. doi: 10.1038/nm.4363. Full text in Research Archive
• Geng, Dawei; Jogsten, Ingrid Ericson; Dunstan, Jody; Hagberg, Jessika; Wang, Thanh & Ruzzin, Jérôme [Show all 8 contributors for this article] (2016). Gas chromatography/atmospheric pressure chemical ionization/mass spectrometry for the analysis of organochlorine pesticides and polychlorinated biphenyls in human serum. Journal of Chromatography A. ISSN 0021-9673. 1453, p. 88–98. doi: 10.1016/j.chroma.2016.05.030. Full text in Research Archive
• Heindel, Jerold J.; Saal, Frederick S. Vom; Blumberg, Bruce; Bovolin, Patrizia; Calamandrei, Gemma & Ceresini, Graziano [Show all 31 contributors for this article] (2015). Parma consensus statement on metabolic disruptors. Environmental health. 14:19. doi: 10.1186/s12940-015-0042-7. Full text in Research Archive Show summary

  A multidisciplinary group of experts gathered in Parma Italy for a workshop hosted by the University of Parma, May 16–18, 2014 to address concerns about the potential relationship between environmental metabolic disrupting chemicals, obesity and related metabolic disorders. The objectives of the workshop were to: 1. Review findings related to the role of environmental chemicals, referred to as “metabolic disruptors”, in obesity and metabolic syndrome with special attention to recent discoveries from animal model and epidemiology studies; 2. Identify conclusions that could be drawn with confidence from existing animal and human data; 3. Develop predictions based on current data; and 4. Identify critical knowledge gaps and areas of uncertainty. The consensus statements are intended to aid in expanding understanding of the role of metabolic disruptors in the obesity and metabolic disease epidemics, to move the field forward by assessing the current state of the science and to identify research needs on the role of environmental chemical exposures in these diseases. We propose broadening the definition of obesogens to that of metabolic disruptors, to encompass chemicals that play a role in altered susceptibility to obesity, diabetes and related metabolic disorders including metabolic syndrome.

• Gauthier, Marie-Soleil; Rabasa-Lhoret, Rémi Rabasa; Prud'homme, Denis; Karelis, Antony D.; Geng, Dawei & Bavel, Bert van [Show all 7 contributors for this article] (2014). The metabolically healthy but obese phenotype is associated with lower plasma levels of persistent organic pollutants as compared to the metabolically abnormal obese phenotype. Journal of Clinical Endocrinology and Metabolism (JCEM). ISSN 0021-972X. 99(6), p. E1061–E1066. doi: 10.1210/jc.2013-3935. Full text in Research Archive
• Ruzzin, Jérôme (2012). Public health concern behind the exposure to persistent organic pollutants and the risk of metabolic diseases. BMC Public Health. 12. doi: 10.1186/1471-2458-12-298. Full text in Research Archive Show summary

  Background: Persistent organic pollutants (POPs) are hazardous chemicals omnipresent in our food chain, which have been internationally regulated to ensure public health. Initially described for their potency to affect reproduction and promote cancer, recent studies have highlighted an unexpected implication of POPs in the development of metabolic diseases like type 2 diabetes and obesity. Based on this novel knowledge, this article aims at stimulating discussion and evaluating the effectiveness of current POP legislation to protect humans against the risk of metabolic diseases. Furthermore, the regulation of POPs in animal food products in the European Union (EU) is addressed, with a special focus on marine food since it may represent a major source of POP exposure to humans. Discussion: There is mounting scientific evidence showing that current POP risk assessment and regulation cannot effectively protect humans against metabolic disorders. Better regulatory control of POPs in dietary products should be of high public health priority. Summary: The general population is exposed to sufficient POPs, both in term of concentration and diversity, to induce metabolic disorders. This situation should attract the greatest attention from the public health and governmental authorities.

• Ruzzin, Jérôme; Lee, Duk-Hee; Carpenter, David O. & Jacobs, David (2012). Reconsidering metabolic diseases: The impacts of persistent organic pollutants. Atherosclerosis. ISSN 0021-9150. 224(1), p. 1–3. doi: 10.1016/j.atherosclerosis.2012.02.039. Full text in Research Archive
• Ibrahim, Mohammad Madani; Fjære, Even; Lock, Erik-Jan; Frøyland, Livar; Jessen, Niels & Lund, Sten [Show all 8 contributors for this article] (2012). Metabolic impacts of high dietary exposure to persistent organic pollutants in mice. Toxicology Letters. ISSN 0378-4274. 215(1), p. 8–15. doi: 10.1016/j.toxlet.2012.09.022. Full text in Research Archive
• Pilon, Geneviève; Ruzzin, Jérôme; Rioux, Laurie Eve; Lavigne, Charles; White, Philip J. & Frøyland, Livar [Show all 10 contributors for this article] (2011). Differential effects of various fish proteins in altering body weight, adiposity, inflammatory status, and insulin sensitivity in high-fat-fed rats. Metabolism: Clinical and Experimental. ISSN 0026-0495. 60(8), p. 1122–1130. doi: 10.1016/j.metabol.2010.12.005. Full text in Research Archive
• Ibrahim, Mohammad Madani; Fjære, Even; Lock, Erik-Jan; Naville, Danielle; Amlund, Heidi & Meugnier, Emmanuelle [Show all 13 contributors for this article] (2011). Chronic Consumption of Farmed Salmon Containing Persistent Organic Pollutants Causes Insulin Resistance and Obesity in Mice. PLOS ONE. 6(9), p. e25170–e25170. doi: 10.1371/journal.pone.0025170. Full text in Research Archive Show summary

  Background: Dietary interventions are critical in the prevention of metabolic diseases. Yet, the effects of fatty fish consumption on type 2 diabetes remain unclear. The aim of this study was to investigate whether a diet containing farmed salmon prevents or contributes to insulin resistance in mice. Methodology/Principal Findings: Adult male C57BL/6J mice were fed control diet (C), a very high-fat diet without or with farmed Atlantic salmon fillet (VHF and VHF/S, respectively), and Western diet without or with farmed Atlantic salmon fillet (WD and WD/S, respectively). Other mice were fed VHF containing farmed salmon fillet with reduced concentrations of persistent organic pollutants (VHF/S-POPs). We assessed body weight gain, fat mass, insulin sensitivity, glucose tolerance, ex vivo muscle glucose uptake, performed histology and immunohistochemistry analysis, and investigated gene and protein expression. In comparison with animals fed VHF and WD, consumption of both VHF/S and WD/S exaggerated insulin resistance, visceral obesity, and glucose intolerance. In addition, the ability of insulin to stimulate Akt phosphorylation and muscle glucose uptake was impaired in mice fed farmed salmon. Relative to VHF/S-fed mice, animals fed VHF/S-POPs had less body burdens of POPs, accumulated less visceral fat, and had reduced mRNA levels of TNFa as well as macrophage infiltration in adipose tissue. VHF/S-POPs-fed mice further exhibited better insulin sensitivity and glucose tolerance than mice fed VHF/S. Conclusions/Significance: Our data indicate that intake of farmed salmon fillet contributes to several metabolic disorders linked to type 2 diabetes and obesity, and suggest a role of POPs in these deleterious effects. Overall, these findings may participate to improve nutritional strategies for the prevention and therapy of insulin resistance.

• Ruzzin, Jérôme; Petersen, Rasmus; Meugnier, Emmanuelle; Madsen, Lise; LOCK, ERIK-JAN & Lillefosse, Haldis Haukås [Show all 19 contributors for this article] (2010). Persistent Organic Pollutant Exposure Leads to Insulin Resistance Syndrome. Environmental Health Perspectives. ISSN 0091-6765. 118(4), p. 465–471. doi: 10.1289/ehp.0901321. Full text in Research Archive

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• Bolann, Bjørn Johan; Huber, Sandra; Ruzzin, Jérôme; Brox, Jan; Huitfeldt, Henrik & Monsen, Anne Lise Bjørke (2017). Er miljøgifter i norsk kosthold skadelig for barn? 137(4), p. 295–297. doi: 10.4045/tidsskr.16.0978. Full text in Research Archive
• Heindel, Jerrold J.; Saal, Frederick S. Vom; Blumberg, Bruce; Bovolin, Patrizia; Calamandrei, Gemma & Ceresini, Graziano [Show all 31 contributors for this article] (2017). Correction to: Parma consensus statement on metabolic disruptors (Environmental Health: A Global Access Science Source (2015) 14:1 (54) DOI: 10.1186/s12940-015-0042-7). Environmental health. 16(1). doi: 10.1186/s12940-017-0343-0. Full text in Research Archive
• Bolann, Bjørn Johan; Huber, Sandra; Ruzzin, Jérôme; Brox, Jan; Huitfeldt, Henrik & Monsen, Anne Lise Bjørke (2017). Miljøgifter i kosten handler om mer enn fisk. Tidsskrift for Den norske legeforening (Tidsskriftet). ISSN 0029-2001. 137(14-15), p. 973–974. doi: 10.4045/tidsskr.17.0521. Full text in Research Archive
• Ruzzin, Jérôme; Bethune, Claudette; Goksøyr, Anders; Hylland, Ketil; Lee, Duk Hee & Jacobs, David R [Show all 7 contributors for this article] (2015). Comment on "Contaminant levels in Norwegian farmed Atlantic salmon (Salmo salar) in the 13-year period from 1999 to 2011" by Nøstbakken et al. Environment International. ISSN 0160-4120. 80, p. 98–99. doi: 10.1016/j.envint.2015.01.003. Full text in Research Archive
• Jacobs, David R. Jr.; Ruzzin, Jérôme & Lee, Duk Hee (2014). Environmental pollutants: Downgrading the fish food stock affects chronic disease risk. Journal of Internal Medicine. ISSN 0954-6820. 276(3), p. 240–242. doi: 10.1111/joim.12205. Full text in Research Archive
• Ruzzin, Jérôme & Jacobs, David (2012). The secret story of fish: decreasing nutritional value due to pollution? British Journal of Nutrition. ISSN 0007-1145. 108(3), p. 397–399. doi: 10.1017/S0007114512002048. Full text in Research Archive
• Aunan, Anine & Ruzzin, Jerome Nicolas Marius (2026). Molecular Mechanisms Preserving Skeletal Muscle Integrity and Capacity to Resist Cancer Cell Colonization. Universitetet i Oslo. ISSN 9788234808753. Full text in Research Archive Show summary

  Preserving skeletal muscle integrity is essential for a healthy life. This thesis investigates the mechanisms underlying skeletal muscle deterioration during physiological aging and cancer-associated cachexia, while also exploring the intrinsic capacity of skeletal muscle to suppress cancer cell proliferation. Findings presented in this work demonstrate that the aryl hydrocarbon receptor (AHR) is required for skeletal muscle homeostasis. Myofiber AHR loss results in skeletal muscle decline in adult mice, while AHR activation with FICZ prevents dexamethasone induced atrophy by stimulating anabolic signaling and suppressing atrogene expression. Furthermore, myofiber AHR loss enhances breast cancer-induced muscle wasting in female mice, indicating that AHR protects skeletal muscle under catabolic stress. In addition, the thesis presents an in vitro co-culture model in which C2C12 myotubes suppress breast cancer cell proliferation and induce a pseudohypoxic transcriptional program. Hypoxia further inhibits cancer cell outgrowth on myotubes, an effect not replicated by myotube-secreted factors alone. Collectively, these findings identify AHR as a key regulator of muscle integrity and implicate hypoxia as a contributor of skeletal muscle cell’s resistance to cancer cell colonization.

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