The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.
Unraveling the Temporal Pattern of Diet-Induced Insulin Resistance in Individual Organs and Cardiac Dysfunction in c57bl/6 Mice
Abstract
Type 2 diabetes is a heterogeneous disease characterized by insulin resistance and altered glucose and lipid metabolism in multiple organs. To understand the complex series of events that occur during the development of obesity-associated diabetes, we examined the temporal pattern of changes in insulin action and glucose metabolism in individual organs during chronic high-fat feeding in C57BL/6 mice. Insulin-stimulated cardiac glucose metabolism was significantly reduced after 1.5 weeks of high-fat feeding, and cardiac insulin resistance was associated with blunted Akt-mediated insulin signaling and GLUT4 levels. Insulin resistance in skeletal muscle, adipose tissue, and liver developed in parallel after 3 weeks of high-fat feeding. Diet-induced whole-body insulin resistance was associated with increased circulating levels of resistin and leptin but unaltered adiponectin levels. High-fat feeding caused insulin resistance in skeletal muscle that was associated with significantly elevated intramuscular fat content. In contrast, diet-induced hepatic insulin resistance developed before a marked increase in intrahepatic triglyceride levels. Cardiac function gradually declined over the course of high-fat feeding, and after 20 weeks of high-fat diet, cardiac dysfunction was associated with mild hyperglycemia, hyperleptinemia, and reduced circulating adiponectin levels. Our findings demonstrate that cardiac insulin resistance is an early adaptive event in response to obesity and develops before changes in whole-body glucose homeostasis. This suggests that obesity-associated defects in cardiac function may not be due to insulin resistance per se but may be attributable to chronic alteration in cardiac glucose and lipid metabolism and circulating adipokines.
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“In contrast, high-fat feeding that is associated with the development of insulin resistance and obesity is associated with development of LV dysfunction in many (269, 273, 296) but not all studies (40).”
From Cardiac remodeling in obesity (2008) · cites this paper as [273]
In the citing paper
“Thus C57BL6 mice when placed on a high-fat diet develop LV dysfunction as evidenced by reduced fractional shortening only after 20 wk of high-fat feeding (273).”
From Cardiac remodeling in obesity (2008) · cites this paper as [273]
In the citing paper
“This was addressed by Kim’s group via a high-fat feeding regimen in mice (273). They found that obesity-associated defects in cardiac function did not develop in concert with insulin resistance and concluded that changes in circulating adipokines could be an important contributing factor in cardiac dysfunction.”
From Cardiac remodeling in obesity (2008) · cites this paper as [273]
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BackgroundEarly weaning induces short‐ and long‐term effects on pancreatic islets in Wistar rats of both sexes
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BackgroundEarly overnutrition impairs insulin signaling in the heart of adult Swiss mice
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“One of the HFD-induced metabolic alterations in the heart is an increase in fatty acid oxidation and a reduction in glucose utilization [2,3].”
BackgroundHong, E., Kim, B. W., Jung, D. Y., Kim, J. H., Yu, T. Y., da‐Silva, W. S., Friedline, R. H., Bianco, S. D. C., Seslar, S. P., Wakimoto, H., et al. (2013) · Endocrinology · doi:10.1210/en.2012-2261 · Cited by 23
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“[67] identified C57BL/6 mice to exhibit impaired systolic performance following 20 weeks of HFF as indicated by fractional shortening.”
BackgroundFranekova, V., Angın, Y., Hoebers, N., Coumans, W. A., Simons, P. J., Glatz, J. F. C., Luiken, J. J. F. P., & Larsen, T. S. (2014) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00073.2014 · Cited by 22
“…various diabetic/obese rodent models show impaired insulin signaling, including reduced activation of protein kinase B (Akt/PKB), reduced glucose transporter 4 (GLUT4) translocation from intracellular compartments to the sarcolemma, as well as impaired insulin-induced glucose uptake (10, 35, 37).”
BackgroundRole for hepatic CEACAM1 in regulating fatty acid metabolism along the adipocyte-hepatocyte axis
Russo, L., Ghadieh, H. E., Ghanem, S. S., Al–Share, Q. Y., Smiley, Z. N., Gatto-Weis, C. M., Esakov, E. L., McInerney, M. F., Heinrich, G., Tong, X., et al. (2016) · Journal of Lipid Research · doi:10.1194/jlr.m072066 · Cited by 22
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Modulation of the cardiovascular system by leptin
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“course of chronic high-fat overfeeding induced obesity and anabolic resistance coincides with muscle 480 lipid accumulation (32), but supported by studies showing that diet-induced obesity via high fat 481 feeding in mice can induce insulin resistance after 3 weeks (34) and impair the activation of skeletal 482 muscle…”
BackgroundCellular Protein Quality Control in Diabetic Cardiomyopathy: From Bench to Bedside
Kaur, N., Raja, R., Ruiz‐Velasco, A., & Liu, W. (2020) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2020.585309 · Cited by 24
“As a coping mechanism, hyperinsulinemiainduced ER stress has emerged as a new player in the onset of insulin resistance (70, 71), possibly via IRE1/JNK signaling (58), contributing to reduced cardiac function in T2DM (72).”
BackgroundKim, B. S., Cha, H.-N., Kim, Y., Kim, J., Dan, J., & Park, S. (2009) · Journal of Pharmacological Sciences · doi:10.1254/jphs.09046fp · Cited by 22
Self-citationVileigas, D. F., de Deus, A. F., da Silva, D. C. T., de Tomasi, L. C., de Campos, D. H. S., Adorni, C. S., de Oliveira, S. M., Sant’Ana, P. G., Okoshi, K., Padovani, C. R., et al. (2016) · Physiological Reports · doi:10.14814/phy2.12914 · Cited by 21
“2010), which vary from 8 to 20 weeks of treatment, showed no functional changes; however, other authors reported cardiac dysfunction in mice fed with UHFD for 20 weeks (Park et al. 2005; Cao et al. 2016), as well as Relling et al.”
BackgroundTang, R., Chen, T., & Lin, F. (2021) · ACS Applied Materials & Interfaces · doi:10.1021/acsami.1c17706 · Cited by 22
COMP-angiopoietin-1 enhances skeletal muscle blood flow and insulin sensitivity in mice
Sung, H., Kim, Y., Choi, S. J., Kim, J., Jeune, K. H., Won, K. C., Kim, J. K., Koh, G. Y., & Park, S. (2009) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00122.2009 · Cited by 21
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“A high-fat diet (HFD) induced myocardial insulin resistance in C57BL/6 mice within ten days [68].”
BackgroundInfluentialGrice, B. A., Barton, K. J., Covert, J. D., Kreilach, A. M., Tackett, L., Brozinick, J. T., & Elmendorf, J. S. (2019) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00396.2018 · Cited by 23
“Although muscle maintains normal expression levels of GLUT4 during the first 3–4 wk of HF feeding (19), GLUT4 regulation and glucose transport are nearly maximally impaired in skeletal and cardiac muscle and adipose tissue by 3 wk of HF feeding (37).”
BackgroundPalanivel, R., Vu, V. P., Park, M. S., Fang, X., & Sweeney, G. (2008) · Journal of Endocrinology · doi:10.1677/joe-08-0336 · Cited by 21
“…199, 389–397 An & Rodrigues 2006), and have more recently been observed in ob/ob or db/db mouse and Zucker rat hearts prior to the onset of hyperglycemia and as early as 10 days after the initiation of high-fat feeding (Buchanan et al. 2005, Golfman et al. 2005, Park et al. 2005, Wang et al. 2005).”
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Regulation of Insulin Clearance by Non-Esterified Fatty Acids
Najjar, S. M., Abdolahipour, R., Ghadieh, H. E., Jahromi, M. S., Najjar, J. A., Abuamreh, B. A. M., Zaidi, S., Kumarasamy, S., & Muturi, H. T. (2022) · Biomedicines · doi:10.3390/biomedicines10081899 · Cited by 22
“However, we [25] and others [80,81] have shown that insulin resistance in liver begins shortly after the initiation of high fat intake in a linear relationship with increased lipolysis and NEFA mobilization out of adipocytes, independently of inflammation.”
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“Direct effects of increased body weight are supported by findings in obese mice showing ventricular hypertrophy and dilation (5,6), which did not occur when energy intake was restricted (5).”
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“Several studies have demonstrated that HF diet‐induced obesity in mice is associated with cardiac dysfunction (Ceylan‐Isik et al., 2013; Park et al., 2005).”
BackgroundThe Use of SGLT-2 Inhibitors in Type 2 Diabetes and Heart Failure
Riggs, K. A., Ali, H., Taegtmeyer, H., & Gutierrez, A. (2015) · Metabolic Syndrome and Related Disorders · doi:10.1089/met.2015.0038 · Cited by 20
“Notably, insulin is a key regulator of myocardial substrate metabolism, and defective insulin signaling might exacerbate cardiac lipotoxicity.(26,27) Lipid accumulation leads to cardiomyocte insulin resistance resulting in increased utilization of fatty acids for cardiac energy, decreased contractive response to insul…”
BackgroundElnwasany, A., Ewida, H. A., Szweda, P. A., & Szweda, L. I. (2023) · Antioxidants · doi:10.3390/antiox12030756 · Cited by 20
Automated qualitative batch measurement of lipid droplets in the liver of bird using ImageJ
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“This vicious cycle is reinforced by the development of insulin resistance in white adipose tissue and the large-scale release of free fatty acids, which build up in the peripheral tissues.(9,10) Therefore, it is critical to establish the degree of lipid build-up in organs like the liver and muscle in order to comprehe…”
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Self-citationObesity and Preclinical Changes of Cardiac Geometry and Function
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“The local and systemic factors of the adipose tissue, such as insulin resistance (IR) (21), renin-angiotensin-aldosterone system (RAAS) activation (22), lipotoxicity (23), and interstitial fibrosis (24), may indirectly contribute to the development of CVD.”
BackgroundDiscovery of Novel Anti-Diabetic Drugs by Targeting Lipid Metabolism
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Chronic High-Fat Diet Exacerbates Sexually Dimorphic Pomctm1/tm1 Mouse Obesity
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“…models showed weakened insulin signaling, including reduced activation of protein kinase B (Akt/PKB), reduced glucose transporter 4 (GLUT4) translocation from intracellular compartments to the sarcolemma, as well as impaired insulin-induced glucose uptake (Desrois et al., 2004; Park et al., 2005).”
BackgroundHaggerty, C. M., Mattingly, A. C., Kramer, S. P., Friday, C. M., Jing, L., Suever, J. D., Powell, D. K., Charnigo, R. J., Epstein, F. H., & Fornwalt, B. K. (2015) · Journal of Cardiovascular Magnetic Resonance · doi:10.1186/s12968-015-0180-7 · Cited by 14
“Prior studies have similarly reported acute changes in glucose tolerance [45].”
Metadata
- Authors
- Park, S.-Y., Cho, Y.-R., Kim, H.-J., Higashimori, T., Danton, C., Lee, M.-K., Dey, A., Rothermel, B., Kim, Y.-B., Kalinowski, A., Russell, K. S., & Kim, J. K.
- Affiliations
- Yale University (US)
- The University of Texas Southwestern Medical Center (US)
- Beth Israel Deaconess Medical Center (US)
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2005-12-01
- Volume
- 54
- Issue
- 12
- Pages
- 3530-3540
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2144568374
- Cited by
- 286
- References
- 58
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 6 · 2022: 7 · 2021: 14 · 2020: 14 · 2019: 11 · 2018: 8 · 2017: 16 · 2016: 17 · 2015: 24 · 2014: 21 · 2013: 29 · 2012: 20
- FWCI
- 9.37
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- Robert E. Leet and Clara Guthrie Patterson Trust
- American Heart Association
- National Institutes of Health (5r01hl072016-10)
- U.S. Public Health Service
- National Heart, Lung, and Blood Institute (R01 HL-072016)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK45735, U24DK59635, U24DK059635, U24-DK59635-P, P30DK045735)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Keywords
- insulin resistance, cardiac insulin resistance, high-fat diet, obesity, type 2 diabetes, cardiac glucose metabolism, Akt signaling, GLUT4, skeletal muscle insulin resistance, hepatic insulin resistance, adipose tissue insulin resistance, resistin, leptin, adiponectin, intramuscular fat, intrahepatic triglyceride, cardiac dysfunction, C57BL/6 mice
- MeSH terms
- Adipose Tissue, Animals, Animal Feed, Blood Glucose, Dietary Fats, Glucose, Heart, Heart Diseases, Insulin, Insulin Resistance, Mice, Inbred C57BL, Myocardium, Organ Specificity, Glucose Clamp Technique, Mice
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