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Chad Hancock

Associate Professor
Nutrition, Dietetics & Food Science

S 245 ESC
Provo, UT 84602

Biography

Research Interests


My research focus is on metabolic pathways impacted by changes in energy supply and demands. Factors that contribute to insulin resistance and type 2 diabetes are most often a result of a mismatch between metabolic fuel supply (the food energy that we eat) and metabolic fuel demands (the food and stored energy that we burn through activity). We study energy metabolism and factors contributing to the development of insulin resistance using nutritional, exercise and pharmaceutical approaches.

Our general research objectives include the following:

  • Understand mechanisms by which lifestyle and other factors contribute to the development of insulin resistance.
  • Investigate the effects of different bioactive compounds on glucose management and energy metabolism.
  • Explore mechanisms by which various bioactive compounds impact glucose management and energy metabolism.

This research is vitally important to gain a better understanding of the metabolic problems that underpin many chronic diseases impacted by insulin resistance. We expect our work can lead to improved prevention and therapy for diabetes and related disease conditions.

Recent projects of interest include:

  • A study looking at the effect of dietary selenium and/or increased isoflavones on insulin resistance and baseline glucose management.
  • A study examining the effect of caloric restriction on mitochondrial content.
  • A study examining the effect of iron deficiency and specific enzymatic responses to this energy challenge.
  • A study examining the effect of high fat diets as well as the activation of a critical enzyme involved in energy sensing (AMPK) on muscle mitochondrial content and capacity.
  • A study looking at the effect of high fat diets and activating AMPK on liver fat accumulation.

Current projects of interest include:

  • Examining a potential role of cellular iron dysregulation and insulin resistance.
  • Exploring the effects of specific bioactive compounds on muscle and hepatic iron metabolism.
  • We are examining the possibility that some anti-diabetic therapies may be effective at reducing unwanted toxicities associated with certain chemotherapeutic treatments.
  • Exploring the impact of different dietary bioactive compounds on mitochondrial function and the generation of reactive oxygen species.

Experience

Academic - Post-Secondary

  • Associate Professor, NDFS, 2014-Present

Professional

  • Assistant Professor, NDFS, 2008-2014
  • Instructor-Nutrition and Dietetics, St. Louis University-Doisy College of Health Sciences, 2008-2008
  • Editorial Board Member, American Journal of Physiology-Endocrinology and Metabolism, 2007-2008
  • Postdoctoral Fellow, Washington University in St. Louis-School of Medicine, 2005-2008

Memberships

  • American Diabetes Association, 2008-Present
  • The American Physiological Society, 2008-Present

Honors & Awards

  • American Physiological Society : APS Publications 2015 Star Reviewer

Courses Taught
Winter 2019

  • NDFS 100: Essentials of Human Nutrition Section 003
  • NDFS 310: Nutr & Metab Sports Exercise Section 001
  • NDFS 494R: Undergrad Research in N D F S Section 007
  • NDFS 602: Advanced Human Nutrition 2 Section 002
  • NDFS 691R: Graduate Seminar Section 001

Fall 2018

  • NDFS 310: Nutr & Metab Sports Exercise Section 001
  • NDFS 494R: Undergrad Research in N D F S Section 005
  • NDFS 691R: Graduate Seminar Section 001

Summer 2018

  • LFSCI 199R: Nonresearch Academic Internshp Section 003
  • NDFS 691R: Graduate Seminar Section 001

Spring 2018

  • NDFS 310: Nutr & Metab Sports Exercise Section 001
  • NDFS 494R: Undergrad Research in N D F S Section 006
  • NDFS 691R: Graduate Seminar Section 001

Research Interests

My research focus is on metabolic pathways impacted by changes in energy supply and demands. Factors that contribute to insulin resistance and type 2 diabetes are most often a result of a mismatch between metabolic fuel supply (the food energy that we eat) and metabolic fuel demands (the food and stored energy that we burn through activity). We study energy metabolism and factors contributing to the development of insulin resistance using nutritional, exercise and pharmaceutical approaches.
Our general research objectives include the following:
• Understand mechanisms by which lifestyle and other factors contribute to the development of insulin resistance.
• Investigate the effects of different bioactive compounds on glucose management and energy metabolism.
• Explore mechanisms by which various bioactive compounds impact glucose management and energy metabolism.
This research is vitally important to gain a better understanding of the metabolic problems that underpin many chronic diseases impacted by insulin resistance. We expect our work can lead to improved prevention and therapy for diabetes and related disease conditions.
Recent projects of interest include:
• A study looking at the effect of dietary selenium and/or increased isoflavones on insulin resistance and baseline glucose management.
• A study examining the effect of caloric restriction on mitochondrial content.
• A study examining the effect of iron deficiency and specific enzymatic responses to this energy challenge.
• A study examining the effect of high fat diets as well as the activation of a critical enzyme involved in energy sensing (AMPK) on muscle mitochondrial content and capacity.
• A study looking at the effect of high fat diets and activating AMPK on liver fat accumulation.
Current projects of interest include:
• Examining a potential role of cellular iron dysregulation and insulin resistance.
• Exploring the effects of specific bioactive compounds on muscle and hepatic iron metabolism.
• We are examining the possibility that some anti-diabetic therapies may be effective at reducing unwanted toxicities associated with certain chemotherapeutic treatments.
• Exploring the impact of different dietary bioactive compounds on mitochondrial function and the generation of reactive oxygen species.

Honors and Awards

  • APS Publications 2015 Star Reviewer

Memberships

  • American Diabetes Association: ( - Present)
  • The American Physiological Society: ( - Present)

Professional Citizenship

  • Other, International Journal of Molecular Sciences, 2019-04-01 - 2019-04-30 - Present
  • Editorial Review Board Member, American Journal of Physiology-Endocrinology and Metabolism, 2008-01-01 - 2008-12-31 - Present
  • Grant Proposal Reviewer, External, NIH, 2015-09-01 - 2015-09-30 - 2015-11-01 - 2015-11-30
  • Other, Missouri State University, 2015-09-01 - 2015-09-30 - 2015-10-01 - 2015-10-31

Courses Taught

2020

  • NDFS 100 : Section 008
  • NDFS 699R: Section 004
  • NDFS 310 : Section 001
  • NDFS 494R: Section 004
  • NDFS 699R: Section 003
  • NDFS 699R: Section 004
  • NDFS 631R: Section 001
  • NDFS 601 : Section 001
  • NDFS 310 : Section 001
  • NDFS 697R: Section 004
  • NDFS 494R: Section 007

2019

  • NDFS 100 : Section 010
  • NDFS 310 : Section 001
  • NDFS 494R: Section 005
  • NDFS 494R: Section 010
  • NDFS 310 : Section 001
  • NDFS 494R: Section 006
  • NDFS 494R: Section 013
  • NDFS 602 : Section 002
  • NDFS 100 : Section 003
  • NDFS 691R: Section 001
  • NDFS 310 : Section 001
  • NDFS 494R: Section 007

2018

  • NDFS 691R: Section 001
  • NDFS 310 : Section 001
  • NDFS 494R: Section 005
  • NDFS 691R: Section 001
  • LFSCI 199R: Section 003
  • NDFS 691R: Section 001
  • NDFS 310 : Section 001
  • NDFS 494R: Section 006
  • NDFS 399R: Section 003
  • NDFS 602 : Section 001
  • PDBIO 799R: Section 019
  • NDFS 100 : Section 003
  • NDFS 691R: Section 001
  • NDFS 691R: Section 002
  • NDFS 310 : Section 001
  • NDFS 494R: Section 007

2017

  • NDFS 601 : Section 001
  • PDBIO 799R: Section 1
  • NDFS 691R: Section 001
  • NDFS 310 : Section 001
  • NDFS 494R: Section 005
  • PDBIO 799R: Section 7
  • NDFS 691R: Section 1
  • NDFS 691R: Section 2
  • PDBIO 799R: Section 002
  • NDFS 691R: Section 1
  • NDFS 310 : Section 001
  • NDFS 494R: Section 6
  • NDFS 602 : Section 001
  • NDFS 100 : Section 003
  • NDFS 691R: Section 001
  • NDFS 691R: Section 002
  • NDFS 310 : Section 001
  • NDFS 494R: Section 007

2016

  • NDFS 601 : Section 001
  • NDFS 691R: Section 001
  • NDFS 310 : Section 001
  • NDFS 494R: Section 005
  • NDFS 691R: Section 1
  • NDFS 691R: Section 1
  • NDFS 310 : Section 001
  • NDFS 602 : Section 001
  • NDFS 100 : Section 003
  • NDFS 691R: Section 001
  • NDFS 310 : Section 001
  • NDFS 494R: Section 007

2015

  • NDFS 601: Section 1
  • NDFS 691R: Section 001
  • NDFS 310 : Section 001
  • NDFS 494R: Section 008
  • NDFS 691R: Section 001
  • NDFS 310 : Section 001
  • NDFS 494R: Section 006
  • NDFS 691R: Section 001
  • NDFS 310 : Section 001
  • BIO 100 : Section 011
  • NDFS 494R: Section 009

2014

  • NDFS 602 : Section 001
  • NDFS 691R: Section 001
  • LFSCI 494R: Section 001
  • NDFS 310 : Section 001
  • NDFS 494R: Section 008
  • NDFS 310 : Section 001
  • NDFS 494R: Section 006
  • NDFS 691R: Section 001
  • NDFS 310 : Section 001
  • BIO 100 : Section 011
  • NDFS 494R: Section 009

2013

  • NDFS 601 : Section 001
  • NDFS 691R: Section 001
  • NDFS 310 : Section 001
  • NDFS 494R: Section 008
  • NDFS 310 : Section 001
  • NDFS 494R: Section 006
  • NDFS 602 : Section 001
  • NDFS 691R: Section 001
  • LFSCI 494R: Section 002
  • BIO 100 : Section 008
  • NDFS 310 : Section 001
  • NDFS 494R: Section 009

2012

  • NDFS 691R: Section 001
  • NDFS 310 : Section 001
  • NDFS 494R: Section 009
  • NDFS 310 : Section 001
  • NDFS 494R: Section 006
  • NDFS 602 : Section 001
  • NDFS 691R: Section 001
  • BIO 100 : Section 009
  • NDFS 494R: Section 009

2011

  • NDFS 691R: Section 001
  • LFSCI 494R: Section 005
  • NDFS 310 : Section 001
  • NDFS 494R: Section 009
  • NDFS 691R: Section 001
  • NDFS 310 : Section 001
  • NDFS 494R: Section 006
  • NDFS 602 : Section 001
  • NDFS 691R: Section 001
  • BIO 100 : Section 009
  • NDFS 494R: Section 009

2010

  • NDFS 691R: Section 001
  • NDFS 310 : Section 001
  • NDFS 494R: Section 011
  • NDFS 494R: Section 001
  • NDFS 602 : Section 001
  • BIO 100 : Section 009
  • NDFS 494R: Section 010

2009

  • PDBIO 120 : Section 006
  • NDFS 494R: Section 011
  • LFSCI 494R: Section 015
  • BIO 100 : Section 010
  • NDFS 494R: Section 012

2008

  • LFSCI 494R: Section 027
  • NDFS 494R: Section 013

Publications

  • Koh J, Hancock CR, Han DH, Holloszy JO, Nair KS, Dasari S. March 19, 2019. AMPK and PPARβ positive feedback loop regulates endurance exercise-mediated GLUT4 expression in skeletal muscle.
  • Mackay AD, Marchant ED, Munk DJ, Watt RK, Hansen JM, Thomson DM, Hancock CR. March 19, 2019. Multi-Tissue Analysis of Exercise or Metformin on Doxorubicin-Induced Iron Dysregulation.
  • Kener KB, Munk DJ, Hancock CR, Tessem JS. January (1st Quarter/Winter) 23, 2018. High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds.
  • Tueller DJ, Harley JS, Hancock CR. August, 2017. Effects of curcumin and ursolic acid on the mitochondrial coupling efficiency and hydrogen peroxide emission of intact skeletal myoblasts.
  • Koh JH, Hancock CR, Terada S, Higashida K, Holloszy JO, Han DH. May 2, 2017. PPARβ Is Essential for Maintaining Normal Levels of PGC-1α and Mitochondria and for the Increase in Muscle Mitochondria Induced by Exercise.
  • 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.
  • Chen T, Moore TM, Ebbert MT, McVey NL, Madsen SR, Hallowell DM, Harris AM, Mackay RP, Char RE, Hancock CR, et alJanuary (1st Quarter/Winter), 2016. Liver kinase B1 inhibits the expression of inflammation-related genes post-contraction in skeletal muscle. 8th ed.
  • Hardman SE, Hall DE, Cabrera AJ, Hancock CR, Thomson DM. April (2nd Quarter/Spring) 18, 2014. The effects of age and muscle contraction on AMPK activity and heterotrimer composition.
  • Stallings MT, Cardon BR, Hardman JM, Bliss TA, Brunson SE, Hart CM, Swiss MD, Hepworth SD, Christensen MJ, Hancock CR. March 10, 2014. A high isoflavone diet decreases 5′ adenosine monophosphate–activated protein kinase activation and does not correct selenium-induced elevations in fasting blood glucose in mice.
  • Bridgewater LC, Mayo JL, Evanson BG, Whitt ME, Dean SA, Yates JD, Holden DN, Schmidt AD, Fox CL, Dhunghel S, et alNovember, 2013. A novel bone morphogenetic protein 2 mutant mouse, nBmp2NLStm, displays impaired intracellular Ca2+ handling in skeletal muscle .
  • Henriksen BS, Curtis ME, Fillmore N, Cardon BR, Thomson DM, Hancock CR. May 31, 2013. The effects of chronic AMPK activation on hepatic triglyceride accumulation and glycerol 3-phosphate acyltransferase activity with high fat feeding. 1st ed.
  • Merrill JF, Thomson DM, Hardman SE, Hepworth SD, Willie S, Hancock CR. November, 2012. Iron deficiency causes a shift in AMP-activated protein kinase (AMPK) subunit composition in rat skeletal muscle. 1st 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.
  • Han D, Hancock CR, Jung SR, Higashida K, Kim SH, Holloszy JO. May, 2011. Deficiency of the mitochondrial electron transport chain in muscle does not cause insulin resistance. 5th ed.
  • Brown JD, Hancock CR, Mongillo AD, Barton BJ, Digiovanni RA, Parcell AC, Winder WW, Thomson DM. April (2nd Quarter/Spring), 2011. Effect of LKB1 deficiency on mitochondrial content, fiber type, and muscle performance in the mouse diaphragm. 4th ed.
  • Hancock CR, Han DH, Higashida K, Kim SH, Holloszy JO. November, 2010. Does calorie restriction induce mitochondrial biogenesis? A reevaluation.
  • Thomson DM, Hancock CR, Evanson BG, Kenney SG, Mallan BB, Mongillo AD, Brown JD, Hepworth S, Fillmore N, Parcell AC, et alJune, 2010. Skeletal muscle dysfunction in muscle-specific LKB1 knockout mice.

Presentations

  • Marchant ED, Marchant ND, Hyldahl RD, Gifford JR, Smith MW, Hancock CR. Investigation of skeletal muscle mitochondrial function following and ultramarathon: a case study in monozygotic twins. Integrative Physiology of Exercise 2020 conference. November, 2020.
  • Jacobsen, Gardner, Handley C, Smith M, Christensen WA, Hancock CR, Joseph P, LeCheminant JD. Effect of 2 years of Caloric Restriction on Perceived Body Shape: The CALERIE Study. The Obesity Society. November, 2020.
  • McCleary M, Gardner A, Jefferies LK, Larson MJ, Hancock CR, Fullmer S, LeCheminant J. Comparing the effects of artificial sweetener and sucrose on cognition. Annual Utah Conference on Undergraduate Research . April, 2019.
  • McCleary M, Gardner A, Jefferies LK, Larson MJ, Hancock CR, Fullmer S, LeCheminant J. Comparing the effects of artificial sweetener and sucrose on cognition. Life Sciences CURA Poster Presentations. April, 2019.
  • Abbott K, Hafen PS, Bowden J, Lopiano R, Hancock CR, Hyldahl RD. Daily heat treatment maintains mitochondrial function and attenuates atrophy in human skeletal muscle subjected to immobilization. SWACSM. October, 2018.
  • Hyldahl RD, Gifford JR, Parcell AC, Hancock CR, Davidson LE, Mack GW. Physiological assessment of a 16-day, 4,385 km ultra-endurance mountain bike race: a case study. SWACSM. October, 2018.
  • Anderson JG, Symkins DD, Hans RC, Hancock CR. Curcumin Alters Iron Regulation in C2C12 Skeletal Muscle Cells and Prevents Iron Accumulation in a Model of Elevated Oxidative Stress. Experimental Biology. April, 2018.
  • Marchant ED, Mackay AD, Munk DJ, Hancock CR. Exercise or Metformin Modulates Doxorubicin Mediated Iron Dysregulation in Liver, Heart and Skeletal Muscle. Experimental Biology. April, 2018.
  • Mackay AD, Hancock CR. Exercise, but Not Metformin Prevents Muscle Function Loss Due to Doxorubicin in Mice Using an in-Situ Model . Experimental Biology. April, 2018.
  • 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.
  • Anderson JG, Hans RC, Symkins DD, Hancock CR. Hydrogen Peroxide Causes Iron Dysregulation in C2C12 Skeletal Muscle Cells. Experimental Biology. April, 2018.
  • Harley JS, Mackay AD, Hancock CR. Metformin Restores Doxorubicin Induced Reduction in Complex II Respiration in C2C12 Skeletal Muscle Myotubes. 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.
  • Anderson JG, Munk DJ, Johnson JM, Wright DC, Hancock CR. Hepatic Iron Regulation in Two Models of Insulin Resistance. American Diabetes Association-Scientific Sessions. June, 2017.
  • Hafen PS, Hancock CR, Hyldahl RD. Deep tissue heating increases mitochondrial respiratory capacity of human skeletal muscle. ACSM National Meeting. May, 2017.
  • Klabacka R, Crandall A, Anderson J, Wright DC, Hancock CR. Analysis of Iron Dysregulation in High-Fat and Iron Deficient Rat Models. Experimental Biology. April, 2016.
  • Louw MJ, Crandall AD, Murphy TS, Reynolds MS, Bernhisel D, Hancock CR. Exercise Limits Loss of Respiratory Function Seen with Doxorubicin Treatment without Affecting Muscle Function. Experimental Biology. April, 2016.
  • Murphy TS, Crandall AD, Louw MJ, Bernhisel D, Reynolds M, Hancock CR. Metformin Limits Loss of Mitochondrial Respiration Seen With Doxorubicin Treatment Without Affecting Muscle Function . Experimental Biology. April, 2016.
  • JOHNSON JM, SMITH DH, WRIGHT DC, WATT R, Hancock CR. Rosiglitazone Ameliorates Iron Dysregulation in Livers from ZDF Rats. American Diabetes Association-Scientific Sessions. June, 2015.
  • Johnson JM, Smith D, Watt RK, Wright DC, Hancock CR. Rosiglitazone ameliorates iron dysregulation inlivers from ZDF rats . Diabetes Scientific Sessions. June, 2015.
  • Mayo JL, Nichols BA, Olsen DS, Cordner RD, Hancock CR, Weber KS, Wilson E, Edwards JG, Barrow JR, Bridgewater LC. The nBMP2 mutant mouse shows defects in intracellular calcium transport-regulated pathways. Southwest Regional Meeting of the Society for Developmental Biology. March, 2014.
  • Hancock CR. “Changes in skeletal muscle oxidative capacity in response to chronic AMPK activation and elevated dietary fat”. Southwest Chapter of the American College of Sports Medicine Meeting. October, 2013.
  • Hardman SE, Merrill JF, Thomson DM, Hancock CR. The effect of iron deficiency on AMPK subunit isoform composition in skeletal muscle. Experimental Biology. April, 2013.
  • Cardon BR, Stallings MT, Brunson SE, Hart CM, Swiss MD, Hepworth SD, Christensen MJ, Hancock CR. Dietary isoflavones and supplemental selenium show interactive effects on blood-glucose homeostasis in male FVB mice. Experimental Biology. Isoflavones and supplemental selenium have shown interactive effects on body weight, body fat, and blood-glucose homeostasis To further elucidate the effects of the interaction, FVB mice were fed either high or low-isoflavone (HIF or LIF) diets, with or without supplemental selenium Custom diets were designed to be equivalent in vitamin, mineral and amino acid profiles, but to differ in soy protein and specific isoflavone content The HIF diet was tested to ensure 500mg/kg aglycone equivalents of genistein + daidzein Selenium was administered by gavage daily (3mg/kg body wt/day) as Se-methylselenocysteine, either from conception (Sel-C), or weaning (Sel-W) All groups were compared against a LIF-no-Sel control group After 5 months HIF-Sel-W mice had elevated fasting glucose levels (HIF-no sel 1062 ± 276, HIF-Sel-W 1216 ± 279 mg/dL, p=008) LIF-Sel-W mice followed the same trend, but values were not significant (p=109) Homeostatic Model Assessment of Insulin Resistance showed a 274% ± 36% increase of insulin resistance in the LIF-Sel-C group (p=034), but not in HIF groups Although blood-glucose and insulin levels were affected by treatments, body weights and abdominal fat pads were not different, contrary to findings in other models These results demonstrate an interactive effect of dietary isoflavone content and supplemental selenium on glucose regulation in the absence of changes in body fat FASEB J March 29, 2012 26:86914. April, 2012.
  • Stallings MT, Hardman JM, Hart CM, Christensen MJ, Hancock CR. Fiber-type skeletal muscle response to dietary selenium and isoflavone supplementation in male mice. Experimental Biology. Previous research has shown selenium (Se) and isoflavone (IF) supplementation influences carbohydrate metabolism and insulin sensitivity In response to different dietary IF contents and/or supplemental Se, we examined adaptations of mitochondrial proteins and FOXO1a in skeletal muscle FOXO1a is a transcription factor that suppresses insulin sensitivity and alters glucose metabolism Male FVB mice were fed diets for six months providing minimal IF or 500 mg/kg equivalents of genistein and daidzein All other dietary components were equivalent Selenium was administered by gavage daily (3mg/kg body wt/day as Se-methylselenocysteine) Results show elevated dietary IF content decreased FOXO1a abundance in Tibialis Anterior (19±47%) and Red Quadriceps (RQ) (17±5%) vs low IF Supplemental Se decreased RQ FOXO1a levels in low IF mice (59±10% vs control; p<0001) Our data show Se also decreases FOXO1a in White Quadriceps (12±4%) and RQ (17±9%) vs no Se overall As Se had the greatest effect by decreasing FOXO1a in the RQ, we investigated changes in mitochondrial content by measuring Uncoupling Protein 3 (UCP3) and Cytochrome C (CytC) in the same muscle Both increased in response to supplemental Se (CytC 126±43%, UCP3 99±315% elevated vs control, p<005) These data suggest fiber-type specific adaptation in response to supplemental Se and elevated dietary isoflavone content FASEB J March 29, 2012 26:108625 . April, 2012.
  • Merrill JF, Hepworth SD, Willie S, Winder WW, Thomson DM, Hancock CR. Iron deficiency causes a shift in AMP-activated protein kinase (AMPK) catalytic subunit composition in rat skeletal muscle. Experimental Biology. To determine effects of iron deficiency on LKB1/AMPK signaling, rats were fed a control (C=029 mg/g Fe) or iron deficient (ID=0 mg/g Fe) diet for 8 wks resulting in hematocrits of 475% ± 10% and 165% ± 06% respectively Iron deficiency resulted in 283% greater muscle fatigue (p<001) in response to 10 min of stimulation (1 twitch/sec) and was associated with a greater reduction in phosphocreatine (C: 456%; ID: 859%) and ATP levels (C: 0%; ID: 240%) AMPK activation increased with stimulation in muscles of C and ID animals A reduction in Cytochrome c and other heme-containing mitochondrial proteins was observed in ID animals (p<001) The two isoforms of the AMPK catalytic subunit (α) are known to sense and respond differently to energy challenges In ID animals, the AMPKα2 subunit protein content was reduced by 284% (p<005), however this did not result in a significant difference in resting AMPKα2 activity AMPKα1 protein was unchanged, however an overall increase in AMPKα1 activity was observed (C: 13758 pmol/mg/min; ID: 22298 pmol/mg/min, p<001) Resting phospho Acetyl CoA Carboxylase (pACC) was also increased by 17-fold (p<005), indicating greater AMPK activity that was not determined by the AMPK activity assay This study indicates that chronic iron deficiency causes a shift in the expression of AMPKα subunit composition and potentially altered sensitivity to cellular energy challenges FASEB J March 29, 2012 26:114412. April, 2012.
  • Curtis M, Henriksen B, Fillmore N, Winder WW, Thomson DM, Hancock CR. Chronic activation of AMPK limits hepatic triglyceride accumulation independent of changes in total glycerol-3-phosphate-acyltransferase activity. Experimental Biology. April, 2011.
  • Thomson DM, Hancock CR, Evanson BG, Kenney SG, Malan BB, Mongillo AD, Brown JD, Hepworth S, Fillmore N, Parcell AC, et alMuscle-specific LKB1 knockout leads to skeletal muscle dysfunction. FASEB Summer Research Conference- AMPK:Central Regulatory System in Metacolism & Growth. October, 2010.
  • Evanson BG, Schmidt AD, Mayo JL, Bridgewater LC, Hancock CR. Nuclear bone morphogenetic protein 2 mutant mice exhibit slowed relaxation and a shift in the force frequency relationship in skeletal muscle. Experimental Biology 2010. . April, 2010.
  • Evanson BG, Hepworth SD, Winder WW, Thomson DM, Hancock CR. MUSCLE SPECIFIC LKB1 DEFICIENCY RESULTS IN SLOWED MUSCLE RELAXATION AND EXAGGERATED FATIGUE. International Biochemistry of Exercise. 2009.
  • Fillmore N, Jacobs DL, Mills D, Winder WW, Hancock CR. Effect of high fat diet and chronic chemical activation of AMPK on skeletal muscle mitochondria. International Conference on Biochemistry of Exercise. Appl Physiol Nutr Metab Vol 34, p 1128, 2009. 2009.
Chad Hancock