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e-Letters: Comments and Responses

Comment on Nolan et al. Insulin Resistance as a Physiological Defense Against Metabolic Stress: Implications for the Management of Subsets of Type 2 Diabetes. Diabetes 2015;64:673–686

  1. Heinrich Taegtmeyer1⇑,
  2. Christophe Beauloye2,
  3. Romain Harmancey3 and
  4. Louis Hue4
  1. 1Division of Cardiovascular Medicine, Department of Internal Medicine, The University of Texas Medical School at Houston, Houston, TX
  2. 2Pôle de Recherche Cardiovasculaire, Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain, Brussels, Belgium
  3. 3Department of Physiology and Biophysics, The University of Mississippi Medical Center, Jackson, MS
  4. 4Protein Phosphorylation Unit, de Duve Institute, Université catholique de Louvain, Brussels, Belgium
  1. Corresponding author: Heinrich Taegtmeyer, heinrich.taegtmeyer{at}uth.tmc.edu.
Diabetes 2015 Oct; 64(10): e37-e37. https://doi.org/10.2337/db15-0655
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We read with much interest the article by Nolan et al. (1) on insulin resistance (IR) as a defense against metabolic stress. This is the third in a cluster of reviews beginning with the hypothesis that IR protects the heart from fuel overload in dysregulated metabolic states (2) and coincides with a review by Connor et al. (3). In our article (2), we stressed the deleterious effects of dysregulated glucose and fat metabolism on the function of the heart and proposed physiologic and biochemical mechanisms by which IR protects the heart from fuel overload. Nolan et al. (1) focused on insulin-induced metabolic stress and expanded on the view that overriding IR with intensive insulin treatment could be harmful (4). Lastly, Connor et al. (3) stressed that many of the adaptations occurring in metabolic diseases characterized by nutritional excess can be viewed as protective in nature rather than pathogenic per se. The observations that excessive insulin signaling exacerbates systolic dysfunction when the heart is subjected to pressure overload (5) and the demonstration that IR improves metabolic and contractile efficiency in the inotropically challenged heart (6) complement each other. Lowering blood glucose levels at all costs may be harmful. We have proposed that in the management of diabetes of patients with heart failure the target should be the source rather than the destination of excess fuel (7). The three reviews and other published work (8) argue in support of the concept that IR is a physiological defense mechanism against metabolic stress. One can only hope that the concept will gain further traction.

Article Information

Duality of Interest. No potential conflicts of interest relevant to this article were reported.

  • © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.

References

  1. ↵
    1. Nolan CJ,
    2. Ruderman NB,
    3. Kahn SE,
    4. Pedersen O,
    5. Prentki M
    . Insulin resistance as a physiological defense against metabolic stress: implications for the management of subsets of type 2 diabetes. Diabetes 2015;64:673–686
    OpenUrlAbstract/FREE Full Text
  2. ↵
    1. Taegtmeyer H,
    2. Beauloye C,
    3. Harmancey R,
    4. Hue L
    . Insulin resistance protects the heart from fuel overload in dysregulated metabolic states. Am J Physiol Heart Circ Physiol 2013;305:H1693–H1697
    OpenUrlAbstract/FREE Full Text
  3. ↵
    1. Connor T,
    2. Martin SD,
    3. Howlett KF,
    4. McGee SL
    . Metabolic remodelling in obesity and type 2 diabetes: pathological or protective mechanisms in response to nutrient excess? Clin Exp Pharmacol Physiol 2015;42:109–115
    OpenUrlCrossRefPubMed
  4. ↵
    1. Nolan CJ,
    2. Ruderman NB,
    3. Prentki M
    . Intensive insulin for type 2 diabetes: the risk of causing harm. Lancet Diabetes Endocrinol 2013;1:9–10
    OpenUrlCrossRefPubMed
  5. ↵
    1. Shimizu I,
    2. Minamino T,
    3. Toko H, et al
    . Excessive cardiac insulin signaling exacerbates systolic dysfunction induced by pressure overload in rodents. J Clin Invest 2010;120:1506–1514
    OpenUrlCrossRefPubMedWeb of Science
  6. ↵
    1. Harmancey R,
    2. Lam TN,
    3. Lubrano GM,
    4. Guthrie PH,
    5. Vela D,
    6. Taegtmeyer H
    . Insulin resistance improves metabolic and contractile efficiency in stressed rat heart. FASEB J 2012;26:3118–3126
    OpenUrlAbstract/FREE Full Text
  7. ↵
    1. Khalaf KI,
    2. Taegtmeyer H
    . After avandia: the use of antidiabetic drugs in patients with heart failure. Tex Heart Inst J 2012;39:174–178
    OpenUrlPubMed
  8. ↵
    1. Agius L
    . High-carbohydrate diets induce hepatic insulin resistance to protect the liver from substrate overload. Biochem Pharmacol 2013;85:306–312
    OpenUrlCrossRefPubMed
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Comment on Nolan et al. Insulin Resistance as a Physiological Defense Against Metabolic Stress: Implications for the Management of Subsets of Type 2 Diabetes. Diabetes 2015;64:673–686
Heinrich Taegtmeyer, Christophe Beauloye, Romain Harmancey, Louis Hue
Diabetes Oct 2015, 64 (10) e37; DOI: 10.2337/db15-0655

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Comment on Nolan et al. Insulin Resistance as a Physiological Defense Against Metabolic Stress: Implications for the Management of Subsets of Type 2 Diabetes. Diabetes 2015;64:673–686
Heinrich Taegtmeyer, Christophe Beauloye, Romain Harmancey, Louis Hue
Diabetes Oct 2015, 64 (10) e37; DOI: 10.2337/db15-0655
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