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Benjamin Bikman

Associate Professor
Physiology & Developmental Biology

3017 LSB
Provo, UT 84602

Biography

Biography
Dr. Bikman’s research focus is to elucidate the molecular mechanisms that mediate the disruption that causes and accompanies metabolic disorders, such as obesity, type 2 diabetes, and dementia. Driven by his academic training (Ph.D. in Bioenergetics and postdoctoral fellowship with the Duke-National University of Singapore in metabolic disorders), he is currently exploring the contrasting roles of insulin and ketones as key drivers of metabolic function. He frequently publishes his research in peer-reviewed journals and presents at international science meetings.

Research Interests
The focus of my lab (the Laboratory of Obesity and Metabolism) is twofold. First, we aim to identify the molecular mechanisms that explain the increased risk of disease that accompanies weight gain, with particular emphasis on the etiology of insulin resistance and disrupted mitochondrial function. Second, we hope to reveal novel cellular processes that are responsible for fat development and accrual, with a particular emphasis on white/brown fat and the contrasting effects of insulin and ketones.

Much of our recent work is focused on the pathogenicity of the hormone insulin. Insulin, while necessary for healthy living, elicits significant and harmful changes in tissue metabolic function when chronically elevated. Several projects have stemmed from this work, including a focus on the varying effects of dietary macronutrients (e.g. carbohydrates vs. fats) on insulin homeostasis, the effects of insulin on brown adipose tissue (and metabolic rate), and insulin-induced brain alterations.

We employ numerous pharmacological and genetic tools to better understand the origins and consequences of ceramide accumulation on various factors related to metabolic function, including signal transduction, substrate utilization, and energy expenditure.

Education

  • Doctor of Philosophy, Bioenergetics, East Carolina University, 2008
  • Master of Science, Exercise Physiology, Brigham Young University, 2005
  • Bachelor of Science, Exercise Science, Brigham Young University, 2003

Experience
Academic - Post-Secondary

  • Postdoctoral Research Fellow, Duke-National University of Singapore Medical School, 2009-2011

Memberships

  • Mitochondrial Physiology Society, 2012-Present
  • The Obesity Society, 2012-Present
  • American Diabetes Association, 2011-Present
  • American Physiological Society, 2010-Present

Honors and Awards

  • Oroboros Instruments : Travel Award
  • Keystone Symposium : Travel Scholarship
  • NIH: Pre-doctoral fellowship

Courses Taught
Winter 2019

  • PDBIO 295R: Introductory Undgrad Research Section 003
  • PDBIO 365: Pathophysiology Section 001
  • PDBIO 495R: Adv Undergraduate Research Section 003
  • PDBIO 550R: Advanced Topics in PDBio Section 003
  • PDBIO 649R: Laboratory Research Section 003
  • PDBIO 699R: Master's Thesis Section 003

Fall 2018

  • PDBIO 495R: Adv Undergraduate Research Section 003
  • PDBIO 699R: Master's Thesis Section 003

Summer 2018

  • PDBIO 295R: Introductory Undgrad Research Section 003
  • PDBIO 495R: Adv Undgraduate Research Section 003
  • PDBIO 498: Advanced Senior Research Section 001
  • PDBIO 550R: Advanced Topics in PDBio Section 003

Spring 2018

  • PDBIO 295R: Introductory Undgrad Research Section 003
  • PDBIO 495R: Adv Undgraduate Research Section 003

Research Interests

The focus of my lab (the Laboratory of Obesity and Metabolism) is twofold. First, we aim to identify the molecular mechanisms that explain the increased risk of disease that accompanies weight gain, with particular emphasis on the etiology of insulin resistance and disrupted mitochondrial function. Second, we hope to reveal novel cellular processes that are responsible for fat development and accrual, with a particular emphasis on white/brown fat and the contrasting effects of insulin and ketones.

Much of our recent work is focused on the pathogenicity of the hormone insulin. Insulin, while necessary for healthy living, elicits significant and harmful changes in tissue metabolic function when chronically elevated. Several projects have stemmed from this work, including a focus on the varying effects of dietary macronutrients (e.g. carbohydrates vs. fats) on insulin homeostasis, the effects of insulin on brown adipose tissue (and metabolic rate), and insulin-induced brain alterations.

We employ numerous pharmacological and genetic tools to better understand the origins and consequences of ceramide accumulation on various factors related to metabolic function, including signal transduction, substrate utilization, and energy expenditure.

Education

  • Doctor of Philosophy, Bioenergetics , institution ( 2008-01-01 - 2008-12-31 )
  • Master of Science, Exercise Physiology , institution ( 2005-01-01 - 2005-12-31 )
  • Bachelor of Science, Exercise Science , institution ( 2003-01-01 - 2003-12-31 )

Honors and Awards

  • Travel Award
  • Travel Scholarship
  • NIH: Pre-doctoral fellowship

Memberships

  • American Society for Investigative Pathology: ( - Present)
  • Mitochondrial Physiology Society: ( - Present)
  • The Obesity Society: ( - Present)
  • American Diabetes Association: ( - Present)
  • American Physiological Society: ( - Present)

Professional Citizenship

  • Committee/Council Member, Duke-NUS Postdoctoral Representative, - Present
  • Editor, Associate Editor, International Journal of Molecular Sciences, 2018-06-01 - 2018-06-30 - Present
  • Other, BYU Diabetes Research Lab, 2016-06-01 - 2016-06-30 - Present
  • Committee/Council Member, American Physiological Society - Integrative Physiology, 2015-06-01 - 2015-06-30 - Present
  • Committee/Council Member, American Physiological Society - Translational Physiology, 2015-04-01 - 2015-04-30 - Present
  • Editor, Associate Editor, Guest Editor, 2016-06-01 - 2016-06-30 - 2017-06-01 - 2017-06-30
  • Conference-Related Role, Keystone Symposium, 2011-04-01 - 2011-04-30 - 2011-04-01 - 2011-04-30

Courses Taught

2020

  • PDBIO 495R: Section 003
  • PDBIO 601 : Section 001
  • PDBIO 799R: Section 003
  • PDBIO 295R: Section 003
  • PDBIO 365 : Section 001
  • PDBIO 455R: Section 001
  • PDBIO 349R: Section 005
  • PDBIO 799R: Section 003
  • PDBIO 799R: Section 003
  • PDBIO 295R: Section 003
  • PDBIO 495R: Section 003
  • PDBIO 295R: Section 003
  • PDBIO 649R: Section 003
  • PDBIO 699R: Section 003
  • PDBIO 365 : Section 001

2019

  • PDBIO 495R: Section 003
  • PDBIO 550R: Section 003
  • PDBIO 601 : Section 001
  • PDBIO 295R: Section 003
  • PDBIO 649R: Section 003
  • PDBIO 495R: Section 003
  • PDBIO 295R: Section 003
  • PDBIO 649R: Section 003
  • PDBIO 649R: Section 003
  • PDBIO 495R: Section 003
  • PDBIO 550R: Section 003
  • PDBIO 295R: Section 003
  • PDBIO 649R: Section 003
  • PDBIO 699R: Section 003
  • PDBIO 365 : Section 001

2018

  • PDBIO 495R: Section 003
  • PDBIO 699R: Section 003
  • PDBIO 495R: Section 003
  • PDBIO 498 : Section 001
  • PDBIO 550R: Section 003
  • PDBIO 295R: Section 003
  • PDBIO 495R: Section 003
  • PDBIO 295R: Section 003
  • PDBIO 495R: Section 003
  • PDBIO 295R: Section 003
  • PDBIO 365 : Section 001

2017

  • PDBIO 495R: Section 004
  • PDBIO 601 : Section 001
  • PDBIO 295R: Section 004
  • PDBIO 365 : Section 002
  • PDBIO 495R: Section 4
  • PDBIO 494R: Section 004
  • PDBIO 495R: Section 004
  • PDBIO 699R: Section 4
  • PDBIO 494R: Section 004
  • PDBIO 495R: Section 004
  • PDBIO 649R: Section 4
  • PDBIO 699R: Section 4
  • PDBIO 365 : Section 001
  • PDBIO 494R: Section 004

2016

  • PDBIO 495R: Section 004
  • PDBIO 601 : Section 001
  • PDBIO 649R: Section 4
  • PDBIO 699R: Section 4
  • PDBIO 365 : Section 002
  • PDBIO 494R: Section 004
  • PDBIO 495R: Section 004
  • PDBIO 494R: Section 4
  • PDBIO 495R: Section 4
  • PDBIO 699R: Section 4
  • PDBIO 494R: Section 004
  • PDBIO 495R: Section 004
  • PDBIO 498: Section 1
  • PDBIO 550R: Section 4
  • PDBIO 649R: Section 4
  • PDBIO 699R: Section 4
  • PDBIO 365 : Section 001
  • PDBIO 494R: Section 004

2015

  • PDBIO 495R: Section 005
  • PDBIO 601 : Section 001
  • PDBIO 699R: Section 5
  • PDBIO 365 : Section 002
  • PDBIO 349R: Section 004
  • PDBIO 494R: Section 005
  • PDBIO 799R: Section 012
  • PDBIO 649R: Section 024
  • PDBIO 494R: Section 026
  • PDBIO 495R: Section 005
  • PDBIO 799R: Section 002
  • PDBIO 494R: Section 005
  • PDBIO 495R: Section 005
  • PDBIO 498 : Section 001
  • PDBIO 550R: Section 005
  • PDBIO 799R: Section 005
  • PDBIO 649R: Section 005
  • PDBIO 699R: Section 005
  • PDBIO 365 : Section 002
  • PDBIO 494R: Section 005

2014

  • PDBIO 495R: Section 005
  • PDBIO 550R: Section 005
  • PDBIO 601 : Section 001
  • PDBIO 799R: Section 005
  • PDBIO 699R: Section 005
  • PDBIO 365 : Section 002
  • PDBIO 494R: Section 005
  • STAC 191 : Section 018
  • PDBIO 495R: Section 026
  • PDBIO 799R: Section 014
  • PDBIO 649R: Section 024
  • PDBIO 495R: Section 005
  • PDBIO 799R: Section 004
  • PDBIO 649R: Section 005
  • PDBIO 495R: Section 005
  • PDBIO 550R: Section 005
  • PDBIO 799R: Section 010
  • PDBIO 649R: Section 005
  • PDBIO 365 : Section 002
  • PDBIO 349R: Section 003
  • PDBIO 650R: Section 001
  • PDBIO 494R: Section 005
  • STAC 191 : Section 018

2013

  • PDBIO 495R: Section 005
  • PDBIO 550R: Section 005
  • PDBIO 799R: Section 011
  • PDBIO 649R: Section 005
  • PDBIO 365 : Section 001
  • PDBIO 349R: Section 004
  • PDBIO 689R: Section 001
  • PDBIO 494R: Section 005
  • STAC 191 : Section 018
  • PDBIO 495R: Section 005
  • PDBIO 649R: Section 005
  • PDBIO 494R: Section 005
  • PDBIO 495R: Section 005
  • PDBIO 649R: Section 005
  • PDBIO 494R: Section 005
  • PDBIO 495R: Section 005
  • PDBIO 498 : Section 002
  • PDBIO 550R: Section 005
  • PDBIO 649R: Section 005
  • PDBIO 365 : Section 002
  • PDBIO 494R: Section 005

2012

  • PDBIO 495R: Section 003
  • PDBIO 550R: Section 003
  • PDBIO 649R: Section 003
  • PDBIO 365 : Section 001
  • PDBIO 349R: Section 002
  • PDBIO 494R: Section 003
  • PDBIO 495R: Section 003
  • PDBIO 649R: Section 003
  • PDBIO 494R: Section 003
  • PDBIO 649R: Section 003
  • PDBIO 494R: Section 003
  • PDBIO 495R: Section 003
  • PDBIO 550R: Section 003
  • PDBIO 649R: Section 003
  • PDBIO 365 : Section 002
  • PDBIO 494R: Section 003

2011

  • PDBIO 495R: Section 018
  • PDBIO 494R: Section 019

Publications

  • Tsai K, Bikman BT, Reynolds P, Arroyo J. December, 2020. Differential expression of mTOR related molecules in the placenta from gestational diabetes mellitus (GDM), intrauterine growth restriction (IUGR) and preeclampsia patients.
  • Walton CM, Jacobsen SM, Dallon BW, Saito ER, Bennett SLH, Davidson LE, Thomson DM, Hyldahl RD, Bikman BT. August 29, 2020. Ketones Elicit Distinct Alterations in Adipose Mitochondrial Bioenergetics. 17th ed.
  • Chen T, Hill JT, Moore TM, ECK C, Olsen ZE, Piorczynski TB, Marriott TD, Tessem JS, Walton CM, Bikman BT, et alApril (2nd Quarter/Spring) 24, 2020. Lack of skeletal muscle liver kinase B1 alters gene expression, mitochondrial content, inflammation and oxidative stress without affecting high-fat diet-induced obesity or insulin resistance. 8th ed.
  • Hirschi KM, KYF T, Davis T, Clark JC, Knowlton MN, Bikman BT, Reynolds PR, Arroyo JA. February 12, 2020. Growth arrest-specific protein-6/AXL signaling induces preeclampsia in rats†. 1st ed.
  • Gibbs JL, Dallon BW, Lewis JB, Walton CM, Arroyo JA, Reynolds PR, Bikman BT. November 9, 2019. Diesel Exhaust Particle Exposure Compromises Alveolar Macrophage Mitochondrial Bioenergetics. 22nd ed.
  • Mejia J, Hirshi K, Tsai K, Long M, Tullis B, Bitter E, Bikman B, Reynolds P, Arroyo JA. October (4th Quarter/Autumn) 23, 2019. Differential placental ceramide levels during gestational diabetes mellitus (GDM). 1st ed.
  • Hirshi K, Tsai K, Davis T, Clark J, Knowlton M, Bikman B, Reynolds P, Arroyo JA. August 5, 2019. Growth Arrest Specific Protein (Gas)-6/AXL Signaling Induces Preeclampsia (PE) in Rats.
  • Pape JA, Newey CR, Burrell HR, Workman A, Perry K, Bikman BT, Bridgewater LC, Grose JH. December 15, 2018. Per-Arnt-Sim Kinase (PASK) Deficiency Increases Cellular Respiration on a Standard Diet and Decreases Liver Triglyceride Accumulation on a Western High-Fat High-Sugar Diet. 12th ed.
  • DeMille D, Pape JA, Bikman BT, Ghassemian M, Grose JH. October (4th Quarter/Autumn) 31, 2018. The Regulation of Cbf1 by PAS Kinase Is a Pivotal Control Point for Lipogenesis Versus Respiration in Saccharomyces cerevisiae.
  • Parker BA, Walton CM, Carr ST, Andrus JL, ECK C, Duplisea MJ, Wilson EK, Draney C, Lathen DR, Kenner KB, et alAugust 1, 2018. β-Hydroxybutyrate Elicits Favorable Mitochondrial Changes in Skeletal Muscle. 8th ed.
  • Dallon BW, Parker BA, Hodson AE, Tippetts TS, Harrison ME, MMA A, Witt JE, Gibbs JL, Gray HM, Sant TM, et alFebruary 9, 2018. Insulin selectively reduces mitochondrial uncoupling in brown adipose tissue in mice. 3rd ed.
  • 4th TJR, Bitner BF, Ray JD, Lathen DR, Smithson AT, Dallon BW, Plowman CJ, Bikman BT, Hansen JM, Dorenkott MR, et alNovember 1, 2017. Monomeric cocoa catechins enhance β-cell function by increasing mitochondrial respiration.
  • Lindsley J, Abali E, Bikman BT, Cline S, Fulton T, Rosenthal O, Uhley V, Weintraut R, Williams P, Wisco JJ, et alOctober (4th Quarter/Autumn), 2017. 1 What nutrition-related knowledge, skills, and attitude should medical students develop? . 4th ed.
  • Banks CJ, Rodriguez NW, Gashler KR, Pandya RR, Mortenson JB, Whited MD, Soderblom EJ, Thompson JW, Moseley MA, Reddi AR, et alSeptember 26, 2017. Acylation of Superoxide Dismutase 1 (SOD1) at K122 Governs SOD1-Mediated Inhibition of Mitochondrial Respiration. 20th ed.
  • Sampson M, Lathen DR, Dallon BW, Draney C, Ray JD, Kener KB, Parker BA, Gibbs JL, Gropp JS, Tessem JS, et alMay, 2017. β-Hydroxybutyrate improves β-cell mitochondrial function and survival. 1st ed.
  • Taylor OJ, Thatcher MO, Carr ST, Gibbs JL, Trumbull AM, Harrison ME, Winden DR, Pearson MJ, Tippetts TS, Holland WL, et alMay 20, 2017. High-Mobility Group Box 1 Disrupts Metabolic Function with Cigarette Smoke Exposure in a Ceramide-Dependent Manner. 5th ed.
  • Napa K, Baeder AC, Witt JE, Rayburn ST, Miller MG, Dallon BW, Gibbs JL, Wilcox SH, Winden DR, Smith JH, et alMay 16, 2017. LPS from P gingivalis Negatively Alters Gingival Cell Mitochondrial Bioenergetics. 2697210th ed.
  • Sanders NT, Dutson DJ, Durrant JW, Lewis JB, Wilcox SH, Winden DR, Arroyo JA, Bikman BT, Reynolds PR. March 31, 2017. Cigarette smoke extract (CSE) induces RAGE-mediated inflammation in the Ca9-22 gingival carcinoma epithelial cell line.
  • Lewis JB, Hirschi KM, Arroyo JA, Bikman BT, Kooyman DL, Reynolds PR. March 17, 2017. Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure. 3rd ed.
  • Reynolds MS, Hancock CR, Ray JD, Kener KB, Draney C, Garland K, Hardman J, Bikman BT, Tessem JS. July (3rd Quarter/Summer) 1, 2016. β-Cell deletion of Nr4a1 and Nr4a3 nuclear receptors impedes mitochondrial respiration and insulin secretion. 1st ed.
  • Baeder AC, Napa K, Richardson ST, Taylor OJ, Andersen SG, Wilcox SH, Winden DR, Reynolds PR, Bikman BT. January (1st Quarter/Winter) 1, 2016. Oral Gingival Cell Cigarette Smoke Exposure Induces Muscle Cell Metabolic Disruption.
  • Hodson AE, Tippetts TS, Bikman BT. December 18, 2015. Insulin treatment increases myocardial ceramide accumulation and disrupts cardiometabolic function. 1st ed.
  • Hansen MES, Simmons KJ, Tippetts TS, Thatcher MO, Saito RR, Hubbard ST, Trumbull AM, Parker BA, Taylor OJ, Bikman BT. October (4th Quarter/Autumn) 29, 2015. Lipopolysaccharide Disrupts Mitochondrial Physiology in Skeletal Muscle via Disparate Effects on Sphingolipid Metabolism.
  • Kwon OS, Tanner RE, Barrows KM, Runtsch M, Symons JD, Jalili T, Bikman BT, McClain DA, O'Connell RM, Drummond MJ. July (3rd Quarter/Summer) 1, 2015. MyD88 regulates physical inactivity-induced skeletal muscle inflammation, ceramide biosynthesis signaling, and glucose intolerance. 1st ed.
  • Nelson MB, Swensen AC, Winden DR, Bodine JS, Bikman BT, Reynolds PR. May 8, 2015. Cardiomyocyte mitochondrial respiration is reduced by receptor for advanced glycation end-product signaling in a ceramide-dependent manner.
  • Gibby J, Njeru D, Cvetko S, Merrill RM, Bikman BT, Gibby W. February 1, 2015. Volumetric analysis of central body fat accurately predicts incidence of diabetes and hypertension in adults. 1st ed.
  • Tippetts TS, Winden DR, Swensen AC, Nelson MB, Thatcher MO, Saito RR, Condie TB, Simmons KJ, Judd AM, Reynolds PR, et alNovember, 2014. Cigarette smoke increases cardiomyocyte ceramide accumulation and inhibits mitochondrial respiration. 1st ed.
  • Thatcher MO, Tippetts TS, Nelson MB, Swensen AC, Winden DR, Hansen ME, Anderson MC, Johnson IE, Porter JP, Reynolds PR, et alNovember 15, 2014. Ceramides mediate cigarette smoke-induced metabolic disruption in mice.
  • DeMille D, Bikman BT, Mathis AD, Prince JT, Mackay JT, Sowa SW, Hall TD, Grose JH. July (3rd Quarter/Summer), 2014. A comprehensive protein-protein interactome for yeast PAS kinase 1 reveals direct inhibition of respiration through the phosphorylation of Cbf1. 14th ed.
  • Hansen ME, Tippetts TS, Moulton ER, Holub ZE, Swensen AC, Prince JT, Bikman BT. May 1, 2014. Insulin Increases Ceramide Synthesis in Skeletal Muscle. Article ID 765784th ed.
  • Smith M, Tippetts T, Brassfield E, Tucker B, Ockey A, Swensen A, Anthonymuthu T, Washburn T, Kane D, Prince JT, et alDecember 1, 2013. Mitochondrial fission mediates ceramide-induced metabolic disruption in skeletal muscle. 3rd ed.
  • Erickson KA, Smith ME, Anthonymuthu TS, Brassfield ES, Tucker BJ, Prince JT, Hancock CR, Bikman BT. November, 2012. AICAR inhibits ceramide biosynthesis in skeletal muscle. 45th ed.
  • Siddique MM, Bikman BT, Wang L, Wenk MW, Summers SA. September, 2012. Ablation of dihydroceramide desaturase confers resistance to Etoposide-induced apoptosis in vitro. 9th ed.
  • Bikman BT, Guan Y, Shui G, M SM, Kim J, Wenk MR, Summers SA. April (2nd Quarter/Spring), 2012. Fenretinide prevents prevents lipid-induced insulin resistance by blocking ceramide biosynthesis.
  • Bikman BT. January (1st Quarter/Winter), 2012. A Role for Sphingolipids in the Pathophysiology of Obesity-induced Inflammation.
  • Bikman BT, Bressler MA. December, 2011. Inflammation and Metabolic Syndrome.
  • Bikman BT, Summers SA. 2011. Ceramides as Modulators of Cellular and Whole-body Metabolism. 11th ed.
  • Holland WL, Bikman BT, Summers SA, al. e. 2011. Lipid-induced insulin resistance mediated by the proinflammatory receptor TLR4 requires saturated fatty acid–induced ceramide biosynthesis in mice. 5th ed.
  • Bikman BT, Summers SA. 2011. Sphingolipids and Hepatic Steatosis.
  • Bikman BT, Dohm GL, Houmard JA. 2010. Lipid-induced insulin resistance is prevented in lean and obese myotubes with AICAR treatment.
  • Bikman BT, Dohm GL. 2010. Metformin Improves Skeletal Muscle Insulin Signaling in Obese Rats in a Fiber-type Dependent Manner.
  • Kane DA, Bikman BT, Neufer PD. 2010. Metformin Selectively Attenuates Mitochondrial H2O2 Emission without Affecting Respiratory Capacity in Skeletal Muscle of Obese Rats. 6th ed.
  • Bikman BT, Summers SA. 2010. Sphingolipids and Hepatic Steatosis.
  • Holland WL, Bikman BT, Summers SA, Scherer PE, al. e. 2010. The Pleiotropic Actions of Adiponectin are Initiated via Receptor-Mediated Activation of Neutral Ceramidase Activity. 1st ed.
  • Bikman BT, Cortright RN. 2009. The effects of intrinsic aerobic capacity and diet on insulin signaling and IKKβ activity in rats.
  • Bikman BT, Dohm GL. 2008. Mechanism(s) for Improved Insulin Sensitivity After Gastric Bypass Surgery.
  • Stob N, Bikman BT, Bell C. 2007. Increased Thermogenic Responsiveness to Intravenous Beta-Adrenergic Stimulation in Habitual Exercisers is Not Related to Skeletal Muscle Beta2-Adrengergic Receptor Density.

Presentations

  • Deru L, Bikman BT, Davidson LE, Tucker LA, Bailey BW. The Effects of Exercise on the Fasting Ketone Production Curve: A Randomized Crossover Study. Obesity Week. November, 2020.
  • Deru L, Bikman BT, Davidson LE, Tucker LA, Bailey BW. Exercise accelerates the production of beta-hydroxy butyrate during a 36-hour fast: A Randomized Crossover Study. Southwest ACSM Annual Meeting. October, 2020.
  • Tessem JS, Yang H, Herring J, Wynn A, Elison W, Walton C, Good L, Marchant E, Marchant N, Bikman BT. Full Body Loss of the Nuclear Hormone Receptor Nr4a3 Induces Diabetes and Glucose Intolerance”. Experimental Biology 2020. May, 2020.
  • Melanson J, Olsen ZE, Walton CM, Bikman BT, Thomson DM. Effect of beta-hydroxybutyrate on myoblast proliferation and differentiation. Experimental Biology. April, 2019.
  • Wynn A, Garland K, Kener K, Weber KS, Bikman BT, Hancock CR, Tessem JS. High Fat Fed Nr4a1 Knock Out Mouse has Significant Modulation of Mitochondrial Respiration Across Various Tissues. Experimental Biology. April, 2018.
  • Garland KS, Kener K, Hancock J, Freitas CMT, Bikman BT, Hancock CR, Weber KS, Tessem JS. The effects of Nr4a1 full-body knockout in mice. Utah Conference on Undergraduate Research. February, 2018.
  • Mejia CA, Appiah MM, Lewis JB, Bikman BT, Hansen JM, Reynolds PR, Arroyo JA. Gas6 reduces cellular respiration and increases reactive oxygen species in immortalized human first trimester trophoblast cells. Experimental Biology. April, 2017.
  • Cho J, Kim JS, Lewis JB, Reynolds PR, Bikman BT, Symons JD. Nasal Administration of Diesel Exhaust Particles Does Not Evoke Dysfunction or Initiate Autophagy in Murine Femoral Arteries. Experimental Biology. April, 2017.
  • Jacobsen CL, Peterson M, Dalanhese DL, Roberts D, Vanmali SN, Sarva S, Witt JE, Wilcox SH, Winden DR, Bikman BT, et alGingival cell mitochondrial bioenergetics are altered with e-cigarette liquid exposure. American Association for Dental Research. March, 2017.
  • Sarva S, Vanmali SN, Dalanhese DL, Peterson M, Jacobsen CL, Hirschi KM, Lewis JB, Wilcox SH, Winden DR, Bikman BT, et alGingival cells exposed to e-cigarette liquid express differential recognition receptors. American Association for Dental Research. March, 2017.
  • Dalanhese DL, Roberts D, Vanmali SN, Peterson M, Jacobsen CL, Sarva S, Hirschi KM, Lewis JB, Wilcox SH, Winden DR, et alGingival cells exposed to e-cigarette liquid induce pro-inflammatory cytokine elaboration. American Association for Dental Research. March, 2017.
  • Pattison J, DeMille D, Bikman BT, Grose JH. The Role of PAS kinase in Cellular Respiration. Utah Conference for Undergraduate Research. PAS kinase is a sensory protein kinase required for glucose homeostasis in yeast, mice and man We recently reported a comprehensive interactome for yeast PAS kinase 1 (Psk1) and confirmed centromere binding factor 1 (Cbf1) as both an in vitro and in vivo substrate The Psk1-dependent phosphorylation and inhibition of Cbf1 decreases cellular respiration through decreased succinate dehydrogenase protein and activity levels while total mitochondrial levels are unaffected In contrast, a significant increase in respiration rate and total mitochondria is seen in PAS kinase-deficient yeast, suggesting that PAS kinase has other downstream targets involved in mitochondrial function This role of PAS kinase appears to be conserved from yeast to mammals in that PAS kinase-deficient mice also have an increased respiration rate, both at the whole animal and cellular level The human Cbf1 homolog (USF1) has been associated with hyperlipidemia suggesting that Cbf1/USF1 allocates glucose towards cellular respiration at the expense of lipogenesis . February, 2017.
  • Ong KL, Rees A, Franson J, White J, Hilton A, Choksi N, Pattison JA, Laub S, Harrison M, Nickle T, et alPAS kinase deficient mice display increased rates of cellular respiration . Keystone Mitochondria Communication. Glucose allocation is an important cellular process that is misregulated in the interrelated diseases obesity, diabetes and cancer Cells have evolved critical mechanisms for regulating glucose allocation, one of which is sensory protein kinases PAS kinase is an evolutionarily conserved sensory protein kinase that regulates glucose allocation in yeast, mice and man (Hao and Rutter, 2008; Grose and Rutter, 2010; Cardon and Rutter, 2012; DeMille and Grose, 2013) PAS kinase deficiency in mice placed on a high-fat diet alters weight gain, liver triglyceride accumulation, insulin-resistance and whole-animal metabolic rate (Hao et al, 2007) Here we report the phenotype of PAS kinase-deficient mice placed on a high-fat high sugar (HFHS) diet, which has been suggested to more closely align with the western diet Although no differences in body weight were observed in this study, PAS kinase deficient mice displayed higher levels of cellular respiration when skeletal muscle or liver cells were assayed, consistent with the whole-animal hypermetabolism previously reported This increased respiration was seen in both the mice placed on standard chow diet as well as on the HFHS diet PAS kinase was recently shown to regulate cellular respiration in yeast as well (DeMille et al, 2014) Combined, these results solidify the evolutionary importance of PAS kinase in the regulation of respiration. January, 2017.
  • Pattison JA, DeMille D, Bikman BT, Grose JH. The role of yeast PAS kinase in controlling cellular respiration through the phosphorylation of USF1/Cbf1. Keystone Mitochondria Communication. A cell’s ability to sense the surrounding nutrients and partition accordingly is crucial to maintaining proper metabolic homeostasis PAS kinase is a highly conserved sensory kinase that plays a crucial role in glucose homeostasis PAS kinase-deficient mice display several phenotypes associated with metabolic disease, including hypermetabolism and resistance to liver triglyceride accumulation when placed on a high fat diet (Hao et al, 2007) However, little is known about the molecular mechanisms involved From a large-scale screen for PAS kinase binding partners, we recently discovered a key substrate of PAS kinase, USF1/Cbf1, that may explain the primary phenotypes of PAS kinase-deficient mice (DeMille et al, 2013) Human alleles of USF1 (Upstream Stimulatory Factor 1) have been shown to be associated with hyperlipidemias in many studies and the yeast homolog, Cbf1, was known to regulate lipids as well Here we provide evidence that both USF1 and Cbf1 also regulate cellular respiration, making USF1/Cbf1 a key switch between lipid and energy production The phosphorylation of Cbf1 by PAS kinase inhibits Cbf1, decreasing lipid biosynthesis while increasing respiration in yeast cells PAS kinase-deficient cells show an increase in overall oxygen consumption as well as succinate dehydrogenase activity and protein levels, while the Cbf1-deficient yeast display several mitochondrial defects PAS kinase regulates a central point in partitioning glucose for lipids or energy production through its regulation of Cbf1/USF1 . January, 2017.
  • Pattison J, DeMille D, Bikman BT, Grose JH. The Role of PAS kinase in Cellular Respiration. LDS Lifescience Research Symposium. PAS kinase is a sensory protein kinase required for glucose homeostasis in yeast, mice and man We recently reported a comprehensive interactome for yeast PAS kinase 1 (Psk1) and confirmed centromere binding factor 1 (Cbf1) as both an in vitro and in vivo substrate The Psk1-dependent phosphorylation and inhibition of Cbf1 decreases cellular respiration through decreased succinate dehydrogenase protein and activity levels while total mitochondrial levels are unaffected In contrast, a significant increase in respiration rate and total mitochondria is seen in PAS kinase-deficient yeast, suggesting that PAS kinase has other downstream targets involved in mitochondrial function This role of PAS kinase appears to be conserved from yeast to mammals in that PAS kinase-deficient mice also have an increased respiration rate, both at the whole animal and cellular level The human Cbf1 homolog (USF1) has been associated with hyperlipidemia suggesting that Cbf1/USF1 allocates glucose towards cellular respiration at the expense of lipogenesis . July, 2016.
  • Bikman BT. Ceramides as mediators of metabolic disruption. ACSM. May, 2016.
  • Laub S, Taylor O, Reynolds PR, Bikman BT. Gingival smoke exposure disrupts skeletal muscle metabolic function. Experimental Biology. April, 2016.
  • Taylor O, Porter M, Reynolds P, Bikman BT. HMGB1 mediates sidestream cigarette smoke-induced metabolic disruption. Experimental Biology. April, 2016.
  • Hodson A, Tippetts T, Bikman BT. Insulin treatment increases myocardial ceramide accumulation and disrupts cardiometabolic function. Experimental Biology. April, 2016.
  • Mejia CA, Monson TD, Jordan CJ, Bikman BT, Reynolds PR, Arroyo JA. Treatment with diet or insulin induces a different placental Ceramide expression during gestational diabetes mellitus (GDM). Experimental Biology. April, 2016.
  • Durrant JW, Gollaher CJ, Sanders NT, Dutson DJ, Lewis JB, Merrill BJ, Milner DC, Christiansen AR, Albright SC, Christiansen CE, et alAvailability of TNF-alpha up-regulates inflammatory RAGE expression by gingival epithelia. American Association for Dental Research. March, 2016.
  • Durrant JW, Gollaher CJ, Sanders NT, Dutson DJ, Lewis JB, Merrill BJ, Milner DC, Christiansen AR, Albright SC, Christiansen CE, et alGingival cells exposed to cigarette smoke extract induce muscle cell metabolic disruption. American Association for Dental Research. March, 2016.
  • Durrant JW, Gollaher CJ, Sanders NT, Dutson DJ, Lewis JB, Merrill BJ, Milner DC, Christiansen AR, Albright SC, Christiansen CE, et alGingival epithelial cells exposed to cigarette smoke extract include RAGE-mediated inflammation. American Association for Dental Research. March, 2016.
  • Grose JH, Bikman BT, Demille D, Pattison J. The role of PAS kinase in controlling cellular respiration . Analytical Genetics. PAS kinase is a sensory protein kinase required for glucose homeostasis in yeast, mice and man We recently reported a comprehensive interactome for yeast PAS kinase 1 (Psk1) and confirmed centromere binding factor 1 (Cbf1) as both an in vivo and in vivo substrate The Psk1-dependent phosphorylation and inhibition of Cbf1 decreases cellular respiration through decreased succinate dehydrogenase protein and activity levels while total mitochondrial levels are unaffected In contrast, a significant increase in respiration rate and total mitochondria is seen in PAS kinase-deficient yeast, suggesting that PAS kinase has other downstream targets involved in mitochondrial function This role of PAS kinase appears to be conserved from yeast to mammals in that PAS kinase-deficient mice also have an increased respiration rate, both at the whole animal and cellular level The human Cbf1 homolog (USF1) has been associated with hyperlipidemia suggesting that Cbf1/USF1 allocates glucose towards cellular respiration at the expense of lipogenesis . January, 2016.
  • Grose JH, Bikman BT, DeMille D. The role of PAS kinase in controlling cellular respiration . Multifaceted Mitochondria. PAS kinase is a sensory protein kinase required for glucose homeostasis in yeast, mice and man We recently reported a comprehensive interactome for yeast PAS kinase 1 (Psk1) and confirmed centromere binding factor 1 (Cbf1) as both an in vivo and in vivo substrate The Psk1-dependent phosphorylation and inhibition of Cbf1 decreases cellular respiration through decreased succinate dehydrogenase protein and activity levels while total mitochondrial levels are unaffected In contrast, a significant increase in respiration rate and total mitochondria is seen in PAS kinase-deficient yeast, suggesting that PAS kinase has other downstream targets involved in mitochondrial function This role of PAS kinase appears to be conserved from yeast to mammals in that PAS kinase-deficient mice also have an increased respiration rate, both at the whole animal and cellular level The human Cbf1 homolog (USF1) has been associated with hyperlipidemia suggesting that Cbf1/USF1 allocates glucose towards cellular respiration at the expense of lipogenesis . June, 2015.
  • Bikman BT. Ceramides are Necessary for Cigarette Smoke-induced Metabolic Disruption. Experimental Biology. April, 2015.
  • Simmons K, Hansen M, Thatcher M, Tippetts T, Bikman BT. Ceramides Mediates Metabolic Disruption with LPS Treatment in Skeletal Muscle. Experimental Biology. April, 2015.
  • Saito R, Simmons K, Hansen M, Thatcher M, Bikman BT. LPS-induced Heart Disruption Requires Ceramides. Experimental Biology. April, 2015.
  • Grose JH, Pattinson J, DeMille D, Bikman BT. The transcription factor centromere binding factor 1 (Cbf1) as a central point of control to upregulate mitochondrial activity and decrease lipid biogenesis in the yeast Saccharomyces cerevisiae”. Tri-Branch ASM Meeting. A cell’s ability to accurately coordinate its growth with nutrient availability is essential for proper metabolic function Nutrient sensing kinases are one mechanism cells have evolved to help sense their surrounding nutrient environment and then properly regulate key pathways PAS kinase is a highly conserved sensory protein kinase required for glucose homeostasis in yeast, mice and man, yet little is known about the molecular mechanisms of its function There is only one well-characterized substrate of PAS kinase, UDP-glucose pyrophosphorylase (Ugp1), a key player in portioning glucose towards cell wall components at the expense of storage We recently identified 106 putative yeast PAS kinase substrates that support its conserved role in glucose homeostasis, and provided in vivo and in vitro evidence for the PAS kinase-dependent phosphorylation of Centromere binding factor 1 (Cbf1) Cbf1 plays an important role in controlling metabolism through the regulation of genes involved in respiration as well as amino acid and lipid biosynthesis We have demonstrated that PAS kinase-dependent phosphorylation inhibits Cbf1, causing decreased respiration in yeast In addition, recent evidence from yeast and mice suggest that Cbf1 and its mammalian homolog, Upstream transcription factor 1 (USF1), play a key role in regulating lipid biosynthesis We have demonstrated that cbf1-deficiency increased the levels of 74 lipids in yeast These results suggest that PAS kinase diverts glucose away from respiration and towards lipid biosynthesis through the phosphorylation and inhibition of Cbf1 Further characterization of PAS kinase binding partners will provide greater insight into how cells regulate fundamental metabolic pathways . April, 2015.
  • Grose JH, Demille D, Bikman BT. The Role of Yeast PAS Kinase in Controlling Cellular Respiration through Cbf1. Tri-Branch ASM Meeting. April, 2015.
  • Bikman BT. Mitochondrial Fission is Necessary for Ceramide-induced Metabolic Disruption. American Diabetes Association. June, 2014.
  • Tippetts T, Winden DR, Wagner M, Condie T, Reynolds PR, Bikman BT. Ceramide is necessary for cigarette smoke-induced reduced heart mitochondrial function. American Diabetes Association. May, 2014.
  • Thatcher M, Tippetts T, Johnson I, Holub Z, Nelson MB, Winden DR, Reynolds PR, Bikman BT. Pulmonary expression and regulation of Cldn6 by tobacco smoke. American Diabetes Association. May, 2014.
  • Nelson MB, Tippetts T, Winden DR, Reynolds PR, Bikman BT. RAGE activation reduces cardiomyocyte mitochondrial function in a ceramide-dependent manner. American Diabetes Association. May, 2014.
  • Bikman BT. Regulators of Muscle Metabolic Function. Utah Vascular Research Laboratory Colloquium Series. November, 2013.
  • Bikman BT. Mitochondrial Fission as a Mediator of Ceramide-induced Metabolic Disruption. Southwest ACSM. October, 2013.
  • Bikman BT, Tucker BJ. Ceramide Increases ROS Generation via Mitochondrial Fission. EB. July, 2013.
  • Bikman BT, Thatcher MO. Ceramide Mediates Cigarette Smoke-induced Insulin Resistance. EB. July, 2013.
  • Bikman BT, Smith ME. Mitochondrial Fission as a Mediator of Ceramide-induced Metabolic Disruption. EB. July, 2013.
  • Bikman BT. Ceramides and Mitochondrial Function. O2K - High Resolution Respirometry. December, 2012.
  • Bikman BT, Erickson KA, Smith ME. AICAR inhibits ceramide biosynthesis in skeletal muscle. Integrative Biology of Exercise. October, 2012.
  • Bikman BT. Dihydroceramide desaturase inhibition prevents ceramide accumulation and improves insulin sensitivity. FASEB Summer Conference - Glucose Transporters, Signaling, and Diabetes. July, 2011.
  • Bikman BT. Fenretinide improves insulin sensitivity by inhibiting dihydroceramide desaturase and preventing ceramide accumulation. Lipid Biology and Lipotoxicity. April, 2011.
  • Bikman BT. Fenretinide improves insulin sensitivity by inhibiting dihydroceramide desaturase and preventing ceramide accumulation. Type 2 Diabetes, insulin resistance, and metabolic function. January, 2011.
Benjamin Bikman