19.02.2025 – 6min

The Expanding Impact of PhenoMaster: Fueling Scientific Discovery

Science thrives on informed choices. Researchers constantly evaluate study designs, methodologies, and the tools they rely on for accurate data. These decisions shape their work, influence collaborations, and ultimately determine the reproducibility and validation of their findings.

A powerful indicator of a technology’s reliability and impact is its presence in high-impact publications. Consistent citations in leading scientific journals solidify a research tool as a gold standard, driving discovery with accurate and reproducible results.

For nearly two decades, PhenoMaster has evolved alongside the scientific community. Starting as a system for monitoring basic metabolic parameters like food and water intake, it has grown into a comprehensive platform for integrating diverse physiological measurements. Today, researchers use PhenoMaster to investigate everything from spontaneous and induced motor behavior (e.g., running wheel) and muscle-specific adaptations (e.g., workload modules) to cognitive function (e.g., operant wall) and complex interactions like the gut-brain axis and oxidative metabolism. Developed in close collaboration with leading scientists, these advancements ensure PhenoMaster remains at the forefront of metabolic research.

This modular design empowers scientists to address increasingly complex biological questions with precision and flexibility. Consequently, PhenoMaster has become a trusted cornerstone of metabolic and phenotypic research at top institutions worldwide.

The Evolution of PhenoMaster Publications

The increasing number of high-impact studies utilizing PhenoMaster demonstrates its expanding role across diverse fields, including metabolism, aging, neurobiology, cancer, and obesity research. To illustrate this growing scientific footprint, let’s examine the trajectory of PhenoMaster citations and highlight some recent discoveries made possible by this platform.

The growth of scientific publications with PhenoMaster throughout the years

We are inspired by the groundbreaking discoveries made possible by PhenoMaster. The diversity of scientific fields it supports and the exceptional quality of research outcomes are truly remarkable. These achievements are consistently recognized in top-tier journals such as Cell, Nature, Nature Metabolism, Molecular Metabolism, Nature Communications, PNAS, iScience, Nature Medicine, and FASEB Journal.

From metabolism and aging to the gut-brain axis, mental health, glycolytic control, and major human pathologies like obesity and NASH, PhenoMaster NG is a trusted resource for cutting-edge research. Its unparalleled reliability, flexibility, and high-throughput capabilities empower scientists to explore the most pressing questions in modern science.

We invite you to explore some of the recent, exciting discoveries enabled by PhenoMaster NG—a platform redefining the boundaries of metabolic phenotypic research. Together, we can continue to drive innovation, solve complex challenges, and advance the frontiers of knowledge.

S. Gallage et al., “A 5:2 intermittent fasting regimen ameliorates NASH and fibrosis and blunts HCC development via hepatic PPARα and PCK1.” Cell Metabolism, vol. 0, no. 0, May 2024, doi: 10.1016/j.cmet.2024.04.015.

Summary: The effects and mechanisms of intermittent fasting (IF) in non-alcoholic steatohepatitis (NASH) and its progression to hepatocellular carcinoma (HCC) were explored in this study. A 5:2 IF regimen was shown to prevent NASH, improve established NASH and fibrosis, and reduce the NASH-to-HCC transition, independent of total calorie intake. The benefits depended on the timing, duration, and frequency of fasting cycles and the type of NASH diet. Mechanistically, PPARα and glucocorticoid signaling, specifically through PCK1, were identified as key mediators of the fasting response, with combined disruption of PPARα and PCK1 abolishing fasting’s protective effects against inflammation and fibrosis.

A. Das et al., “Adenylate cyclase 10 promotes brown adipose tissue thermogenesis.” iScience, p. 111833, Jan. 2025, doi: 10.1016/j.isci.2025.111833.

Summary: Brown adipose tissue (BAT) thermogenesis dissipates energy through heat production, thereby opposing metabolic disease via mitochondrial membrane uncoupling. This study shows that isocitrate dehydrogenase (IDH) activity associated with the expression of mitochondria CO2/bicarbonate sensor ADCY10 plays a key role in brown adipocyte thermogenesis.

A. A. Widjaja et al., “Inhibition of IL-11 signaling extends mammalian healthspan and lifespan.” Nature, pp. 1–9, Jul. 2024, doi: 10.1038/s41586-024-07701-9.

Summary: IL-11, a pro-inflammatory cytokine, promotes aging by regulating the ERK–AMPK–mTORC1 pathway, leading to metabolic decline, frailty, and age-related diseases. Deleting Il11 or blocking IL-11 improves metabolism and muscle function and reduces aging biomarkers, extending lifespan by over 20% in mice. These findings suggest anti-IL-11 therapy, currently in trials for lung disease, could address aging-related pathologies in humans.

P. Zizzari et al., “TGR5 receptors in SF1-expressing neurons of the ventromedial hypothalamus regulate glucose homeostasis.” Mol Metab, p. 102071, Nov. 2024, doi: 10.1016/j.molmet.2024.102071.

Summary: SF1 neurons in the ventromedial hypothalamus regulate food intake, body weight, and glucose metabolism, with some overlapping effects observed by manipulating hypothalamic bile acid receptor TGR5. The authors identified that TGR5 receptors in SF1 neurons promote satiety by adjusting meal patterns in response to metabolic cues and improving whole-body insulin sensitivity. These findings highlight the importance of neuronal TGR5 in energy balance and metabolic regulation.

R. Wang et al., “Adipocyte deletion of the oxygen-sensor PHD2 sustains elevated energy expenditure at thermoneutrality” Nat Commun, vol. 15, no. 1, p. 7483, Aug. 2024, doi: 10.1038/s41467-024-51718-7.

Summary: The thermogenic brown adipose tissue (BAT) effect represents a promising therapeutic strategy for metabolic disease treatment but suffers from the fact that modern human living conditions usually silence BAT function. By impairing the PHD2 pathway, this study shows that this effect can be selectively overcome, opening the door to new therapeutic strategies.

T. Wang et al., “Single-nucleus transcriptomics identifies separate classes of UCP1 and futile cycle adipocytes” Cell Metabolism, vol. 0, no. 0, Jul. 2024, doi: 10.1016/j.cmet.2024.07.005.

Summary: Heat dissipation, a process based on catabolic reaction in adipose tissue, occurs either by uncoupled respiration through uncoupling protein 1 (UCP1) or ATP-dependent futile cycles (FCs), which rely on the mitochondrial membrane potential. Utilizing single-nucleus RNA sequencing and TSE PhenoMaster, this study investigates the heterogeneity of subcutaneous adipose tissue in mice and humans; we identify distinct subpopulations of beige adipocytes and identify a noncanonical thermogenic adipocyte subpopulation, which could be an important regulator of energy homeostasis in mammals.

X. Wang et al., “Adipocyte-derived ferroptotic signaling mitigates obesity” Cell Metabolism, vol. 0, no. 0, Dec. 2024, doi: 10.1016/j.cmet.2024.11.010.

Summary: Ferroptosis, an iron-dependent and lipophilic form of cell death, was suspected to modulate adipose function and activity, particularly in obesity. This study suggests that activating ferroptosis signaling in adipose tissues significantly reduces lipid accumulation in primary adipocytes and might help to prevent and treat obesity and its related metabolic disorders.

Y. Li et al., “Loss of transient receptor potential channel 5 causes obesity and postpartum depression.” Cell, vol. 0, no. 0, Jul. 2024, doi: 10.1016/j.cell.2024.06.001.

Summary: TRPC5 channels detect sensory stimuli and convert them into electrical signals the brain interprets. Using selective manipulation of this channel in hypothalamic oxytocin neurons, notably known to regulate instinctive food seeking and maternal care, this study identifies TRPC5 malfunction as a direct cause of obesity and postpartum depressive behavior phenocopying effect observed in women patients carrying TRPC5 deletion mutation.

L. Ding et al., “Glucose controls lipolysis through Golgi PtdIns4P-mediated regulation of ATGL,” Nat Cell Biol.” pp. 1–15, Apr. 2024, doi: 10.1038/s41556-024-01386-y.

Summary: The metabolic coordination of glucose, amino acids, and fatty acids (FAs) processing is critical for maintaining systemic homeostasis, with disruptions leading to diabetes and metabolic dysfunction-associated steatohepatitis (MASH). While lipolysis is traditionally thought to be hormonally regulated, this study identifies a cell-intrinsic mechanism linking glucose sensing to lipolysis via Golgi PtdIns4P. Inhibiting this pathway improves steatosis symptoms and offers a potential therapeutic approach for MASH and related disorders.

X. Chen et al., “Small extracellular vesicles from young plasma reverse age-related functional declines by improving mitochondrial energy metabolism” Nat Aging, pp. 1–25, Apr. 2024, doi: 10.1038/s43587-024-00612-4.

Summary: Recent studies on heterochronic parabiosis highlight the rejuvenating effects of young blood on aged tissues, though a still unclear mechanism. This study shows that small extracellular vesicles (sEVs) from young mice improve mitochondrial function, reduce aging-related damage, and extend lifespan in aged mice by delivering miRNA cargoes that stimulate PGC-1α expression. Proteomic analyses reveal that young sEVs induce metabolic changes in aged tissues, offering a potential strategy to reverse age-related dysfunction.

Looking Ahead

The growing body of PhenoMaster studies underscores the platform’s vital role in shaping metabolic and phenotypic research. As new challenges arise in precision medicine, aging, and metabolic disorders, reliable and validated tools like PhenoMaster will be essential for pushing the boundaries of scientific discovery.

Let’s continue to advance science together—one study at a time.

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