Education & Certifications


  • BS, The University of Arizona, Chemistry (2021)

All Publications


  • A Leak-Free Head-Out Plethysmography System to Accurately Assess Lung Function in Mice. Journal of applied physiology (Bethesda, Md. : 1985) Bruggink, S., Kentch, K., Kronenfeld, J., Renquist, B. J. 2022

    Abstract

    Mice are a valuable model for elegant studies of complex, systems-dependent diseases, including pulmonary diseases. Current tools to assess lung function in mice are either terminal or lack accuracy. We set out to develop a low-cost, accurate, head-out variable-pressure plethysmography system to allow for repeated, non-terminal measurements of lung function in mice. Current head-out plethysmography systems are limited by air leaks that prevent accurate measures of volume and flow. We designed an inflatable cuff that encompasses the mouse's neck preventing air leak. We wrote corresponding software to collect and analyze the data, remove movement artifacts, and automatically calibrate each dataset. This software calculates inspiratory/expiratory volume, inspiratory/expiratory time, breaths per minute, mid-expiratory flow, and end-inspiratory pause. To validate the use, we established that our plethysmography system accurately measured tidal breathing, the bronchoconstrictive response to methacholine, sex and age associated changes in breathing, and breathing changes associated with house dust mite sensitization. Our estimates of volume, flow, and timing of breaths are in line with published estimates, we observed dose-dependent decreases in volume and flow in response to methacholine (P < 0.05), increased lung volume and decreased breathing rate with aging (P < 0.05), and that house dust mite sensitization decreased volume and flow (P <0.05) while exacerbating the methacholine induced increases in inspiratory and expiratory time (P < 0.05). We describe an accurate, sensitive, low-cost, head-out plethysmography system that allows for longitudinal studies of pulmonary disease in mice.

    View details for DOI 10.1152/japplphysiol.00835.2021

    View details for PubMedID 35608203

  • A critical role of hepatic GABA in the metabolic dysfunction and hyperphagia of obesity CELL REPORTS Geisler, C. E., Ghimire, S., Bruggink, S. M., Miller, K. E., Weninger, S. N., Kronenfeld, J. M., Yoshino, J., Klein, S., Duca, F. A., Renquist, B. J. 2021; 35 (13): 109301

    Abstract

    Hepatic lipid accumulation is a hallmark of type II diabetes (T2D) associated with hyperinsulinemia, insulin resistance, and hyperphagia. Hepatic synthesis of GABA, catalyzed by GABA-transaminase (GABA-T), is upregulated in obese mice. To assess the role of hepatic GABA production in obesity-induced metabolic and energy dysregulation, we treated mice with two pharmacologic GABA-T inhibitors and knocked down hepatic GABA-T expression using an antisense oligonucleotide. Hepatic GABA-T inhibition and knockdown decreased basal hyperinsulinemia and hyperglycemia and improved glucose intolerance. GABA-T knockdown improved insulin sensitivity assessed by hyperinsulinemic-euglycemic clamps in obese mice. Hepatic GABA-T knockdown also decreased food intake and induced weight loss without altering energy expenditure in obese mice. Data from people with obesity support the notion that hepatic GABA production and transport are associated with serum insulin, homeostatic model assessment for insulin resistance (HOMA-IR), T2D, and BMI. These results support a key role for hepatocyte GABA production in the dysfunctional glucoregulation and feeding behavior associated with obesity.

    View details for DOI 10.1016/j.celrep.2021.109301

    View details for Web of Science ID 000668072600010

    View details for PubMedID 34192532

  • Development of a GABA Transaminase Inhibitor That Does Not Penetrate the Blood-Brain Barrier Kronenfeld, J. M. The University of Arizona Honors College. Thesis Repository. 2021
  • Feed intake-dependent and -independent effects of heat stress on lactation and mammary gland development JOURNAL OF DAIRY SCIENCE Xiao, Y., Kronenfeld, J. M., Renquist, B. J. 2020; 103 (12): 12003-12014

    Abstract

    With a growing population, a reliable food supply is increasingly important. Heat stress reduces livestock meat and milk production. Genetic selection of high-producing animals increases endogenous heat production, while climate change increases exogenous heat exposure. Both sources of heat exacerbate the risk of heat-induced depression of production. Rodents are valuable models to understand mechanisms conserved across species. Heat exposure suppresses feed intake across homeothermic species including rodents and production animal species. We assessed the response to early-mid lactation or late-gestation heat exposure on milk production and mammary gland development/function, respectively. Using pair-fed controls we experimentally isolated the feed intake-dependent and -independent effects of heat stress on mammary function and mass. Heat exposure (35°C, relative humidity 50%) decreased daily feed intake. When heat exposure occurred during lactation, hypophagia accounted for approximately 50% of the heat stress-induced hypogalactia. Heat exposure during middle to late gestation suppressed feed intake, which was fully responsible for the lowered mammary gland weight of dams at parturition. However, the impaired mammary gland function in heat-exposed dams measured by metabolic rate and lactogenesis could not be explained by depressed feed consumption. In conclusion, mice recapitulate the depressed milk production and mammary gland development observed in dairy species while providing insight regarding the role of feed intake. This opens the potential to apply genetic, experimental, and pharmacological models unique to mice to identify the mechanism by which heat is limiting animal production.

    View details for DOI 10.3168/jds.2020-18675

    View details for Web of Science ID 000603029300036

    View details for PubMedID 33041042

  • Determining the Role of Obesity and Muscarinic Signaling in Asthma Bruggink, S., Kentch, K., Kronenfeld, J., Renquist, B. WILEY. 2020
  • It's Strong, It's Stable, It's Streptavidin Futch, L., Pham, T., Adamson, B., Reilly, B., Kronenfeld, J., Patterson, K., Inostroza, M., Fraijo, S., Montoya, J., Chavez, R., Hazzard, J. FEDERATION AMER SOC EXP BIOL. 2015