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A recent study employed the Noradrenaline (Norepinephrine) Sensitive ELISA to investigate if over nutrition causes insulin resistance and metabolic disorder through increased sympathetic nervous system activity. Check out the details and access the full findings below.

Abstract

The mechanisms underlying obesity-induced insulin resistance remain incompletely understood, as impaired cellular insulin signaling, traditionally considered the primary driver of insulin resistance, does not always accompany impaired insulin action. Overnutrition rapidly increases plasma norepinephrine (NE), suggesting overactivation of the sympathetic nervous system (SNS). However, the role of the SNS in obesity is controversial, as both increased and decreased SNS activity (SNA) have been reported. Here, we show that reducing catecholamine (CA) release from the SNS protects against overnutrition-induced insulin resistance as well as hyperglucagonemia, adipose tissue dysfunction, and fatty liver disease, as we demonstrate utilizing a mouse model of inducible and peripherally restricted deletion of tyrosine hydroxylase (th; THΔper). A key mechanism through which heightened SNA induces insulin resistance is by triggering adipose tissue lipolysis. Increased SNA emerges as a critical driver in the pathogenesis of overnutrition-induced insulin resistance and metabolic disease independent of cellular insulin signaling.

Sakamoto, Kenichi, et al. “Overnutrition causes insulin resistance and metabolic disorder through increased sympathetic nervous system activity.” Cell Metabolism, vol. 37, no. 1, Jan. 2025, https://doi.org/10.1016/j.cmet.2024.09.012.

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The Mouse Rat 25-OH Vitamin D ELISA Assay Kit was utilized in a recent study! The study focused on how omega-3 fatty acid and vitamin D supplementations partially reverse metabolic disorders and restore gut microbiota in obese wistaria rats. Access the abstract and full text below.

Abstract

Obesity is a global public health issue linked to various comorbidities in both humans and animals. This study investigated the effects of vitamin D (VD) and omega-3 fatty acids (ω3FA) on obesity, gut dysbiosis, and metabolic alterations in Wistar rats. After 13 weeks on a standard (S) or High-Fat, High-Sugar (HFHS) diet, the rats received VD, ω3FA, a combination (VD/ω3), or a control (C) for another 13 weeks. The HFHS diet led to increased weight gain, abdominal circumference, glucose intolerance, insulin resistance, and gut dysbiosis. VD supplementation improved their fasting blood glucose and reduced liver damage, while ω3FA slowed BMI progression, reduced abdominal fat, liver damage, and intestinal permeability, and modulated the gut microbiota. The combination of VD/ω3 prevented weight gain, decreased abdominal circumference, improved glucose tolerance, and reduced triglycerides. This study demonstrates that VD and ω3FA, alone or combined, offer significant benefits in preventing obesity, gut dysbiosis, and metabolic alterations, with the VD/ω3 combination showing the most promise. Further research is needed to explore the mechanisms behind these effects and their long-term potential in both animal and human obesity management.

Le Jan, Dylan, et al. “Omega-3 fatty acid and vitamin D supplementations partially reversed metabolic disorders and restored gut microbiota in obese Wistar rats.” Biology, vol. 13, no. 12, 20 Dec. 2024, p. 1070, https://doi.org/10.3390/biology13121070.

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Sclerostin is a bioactive glycoprotein primarily secreted by osteocytes that plays a crucial role in regulating bone formation and remodeling. It acts as an antagonist of the Wnt/β-catenin signaling pathway, binding to LRP5/6 co-receptors and inhibiting osteoblast activity, thereby reducing bone formation. Because of this regulatory function, sclerostin helps maintain skeletal homeostasis but also contributes to bone loss when present in excess, as seen in conditions like osteoporosis. Its bioactivity has made it a significant therapeutic target—most notably in the development of sclerostin-inhibiting monoclonal antibodies, which enhance bone formation and improve bone mineral density.

Biomedica’s Bioactive Sclerostin ELISA Kit was highlighted in a recent study investigating the association of total and bioactive serum Sclerostin levels with bone metabolism in type 2 diabetes mellitus (T2DM).  Click below for the full publications, where you can find the abstracts and key findings!

Traechslin, Cyril, et al. “Association of total and bioactive serum sclerostin levels with bone metabolism in type 2 diabetes mellitus.” Journal of Clinical & Translational Endocrinology, vol. 40, June 2025, p. 100393, https://doi.org/10.1016/j.jcte.2025.100393.

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Serotonin Sensitive ELISA Kit

Abstract

Introduction: Serotonin (5-HT) is critical for neurodevelopment and the serotonin transporter (SERT) modulates serotonin levels. Perturbed prenatal and postnatal dietary exposures affect the developing offspring predisposing to neurobehavioral disorders in the adult. We hypothesized that the postnatal brain 5-HT-SERT imbalance associated with gut dysbiosis forms the contributing gut-brain axis dependent mechanism responsible for such ultimate phenotypes.

Methods: Employing maternal diet restricted (IUGR, n=8) and high fat+high fructose (HFhf, n=6) dietary modifications, rodent brain serotonin was assessed temporally by ELISA and SERT by quantitative Western blot analysis. Simultaneously, colonic microbiome studies were performed.

Results: At early postnatal (P) day 2 no changes in the IUGR, but a ~24% reduction in serotonin (p = 0.00005) in the HFhf group occurred, particularly in the males (p = 0.000007) revealing a male versus female difference (p = 0.006). No such changes in SERT concentrations emerged. At late P21 the IUGR group reared on HFhf (IUGR/HFhf, (n = 4) diet revealed increased serotonin by ~53% in males (p = 0.0001) and 36% in females (p = 0.023). While only females demonstrated a ~40% decrease in serotonin (p = 0.010), the males only trended lower without a significant change within the HFhf group (p = 0.146). SERT on the other hand was no different in HFhf or IUGR/RC, with only the female IUGR/HFhf revealing a 28% decrease (p = 0.036). In colonic microbiome studies, serotonin-producing Bacteriodes increased with decreased Lactobacillus at P2, while the serotonin-producing Streptococcus species increased in IUGR/HFhf at P21. Sex-specific changes emerged in association with brain serotonin or SERT in the case of Alistipase, Anaeroplasma, Blautia, Doria, Lactococcus, Proteus, and Roseburia genera.

Discussion: We conclude that an imbalanced 5-HT-SERT axis during postnatal brain development is sex-specific and induced by maternal dietary modifications related to postnatal gut dysbiosis. We speculate that these early changes albeit transient may permanently alter critical neural maturational processes affecting circuitry formation, thereby perturbing the neuropsychiatric equipoise.

Ye X et al. (2024) Brain serotonin and serotonin transporter expression in male and female postnatal rat offspring in response to perturbed early life dietary exposures. Front. Neurosci. 18:1363094. doi: 10.3389/fnins.2024.1363094

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The Dopamine Sensitive ELISA Assay was utilized in a recent study! The study explored the effects of probiotics on olanzapine-induced metabolic syndrome through the gut microbiota. For more details, reference the abstract and access to the full text below.

Abstract

Background

Maintaining gut microbial homeostasis is crucial for human health, as imbalances in the gut microbiota (GM) can lead to various diseases, including metabolic syndrome (MS), exacerbated by the use of antipsychotic medications such as olanzapine (OLZ). Understanding the role of the GM in OLZ-induced MS could lead to new therapeutic strategies. This study used metagenomic analysis to explore the impact of OLZ on the GM composition and examined how probiotics can mitigate its adverse effects in a rat model. Changes in weight, blood pressure, and lipid levels, which are key parameters defining MS, were assessed. Additionally, this study investigated serotonin, dopamine, and histopathological changes to explore their possible link with the microbiota-gut-brain axis (MGBA).

Results

OLZ had an antagonistic effect on serotonin and dopamine receptors, and it was consistently found to alter the composition of the GM, with an increase in the relative abundance (RA) of the Firmicutes/Bacteroidetes phyla ratio and TM7 genera, indicating that the anticommonsal action of OLZ affects appetite and energy expenditure, contributing to obesity, dyslipidemia and increased blood pressure, which are core components of MS. Hepatic steatosis and intestinal damage in OLZ-treated rat tissues further indicate its role in MS. Conversely, the administration of probiotics, either alone or in combination with OLZ, was found to mitigate these OLZ-induced symptoms of MS by altering the GM composition. These alterations included increases in the abundances of the taxa Bacteroidetes, Actinobacteria, Prevotella, Blautia, Bacteroides, Bacteroidales, and Ruminococcaceae and a decrease in Firmicute abundance. These changes helped maintain gut barrier integrity and modulated neurotransmitter levels, suggesting that probiotics can counteract the adverse metabolic effects of OLZ by restoring the GM balance. Moreover, this study highlights the modulation of the MGBA by OLZ as a potential mechanism through which probiotics modulate serotonin and dopamine levels, influencing metabolic health.

Conclusion

These findings emphasise the significant impact of OLZ on the GM and its contribution to MS. These findings suggest that interventions targeting the GM, such as probiotics, could mitigate the metabolic side effects of OLZ. Future research should focus on developing integrative treatment approaches that consider the health of the gut microbiome in managing antipsychotic-induced adverse effects.

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The Calprotectin ELISA Kit was utilized in a recent publication. Scientists investigated the impact of repeated microbiome elimination on intestinal immunity and disease susceptibility. Check out the abstract and access to the full text below.

Abstract

Chronic gastrointestinal diseases are a significant global health burden that can require the use of gastrointestinal-cleansing regimens for diagnostics or therapeutic treatment. These regimens are beneficial for facilitating surgical preparation, drug delivery, colorectal cancer screenings, and personal use is common among proponents of natural health and among certain populations at high risk of HIV acquisition. It remains unclear, however, whether repeated clearance of the colonic microbiome induces persistent changes in the microbiome, intestinal immunity, and viral disease susceptibility. We addressed these parameters by repeatedly administering iso-osmolar enemas to rhesus macaques prior to low-dose intra-rectal challenge with simian immunodeficiency virus (SIV). Considering both longitudinal and cross-sectional analyses, we observed no consistent changes in the fecal microbiome or intestinal immune parameters of treated animals, nor were significant differences observed in susceptibility to SIV acquisition. Unexpectedly, enema-treated animals exhibited significantly lower setpoint viral loads after infection, although we were unable to clearly identify attributing causes. Our study demonstrates that repeated microbiome clearance using clinically administered iso-osmolar enemas is not sufficient to restructure the fecal microbiome, perturb intestinal immune parameters, or increase susceptibility to mucosal SIV challenge. This research framework serves as a model for the development of colonic-administered diagnostics and interventions.

Ortiz, Alexandra M. et al. Repeated enema administration in rhesus macaques is not sufficient to promote bacterial dysbiosis or gastrointestinal dysfunction. Mucosal Immunology, Volume 0, Issue 0. doi: 10.1016/j.mucimm.2025.06.002

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