Morphological and functional characterization of diabetic cardiomyopathy in db/db mice following exercise, metformin alone, or combination treatments

Lu, Jiao; Liu, Jingjing; Zhang, Liumei; Wang, Xueqi; Zhang, Yuan; Tang, Qiang

doi:10.1016/j.bbrc.2021.11.018

Cited by 9 publications

(4 citation statements)

References 23 publications

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“…Our data demonstrate no effect of metformin on the body weight of our HFHSD + MET mice, in accordance with Silamikele et al [ 23 ]. However, body weight was reported to be decreased by metformin in other studies [ 24 , 25 ]. Interestingly, similar controversial effects of metformin, oscillating between weight-neutral or weight-sparing effect, have been observed in diabetic patients [ 26 ].…”

Section: Discussionmentioning

confidence: 94%

Effect of Metformin on T2D-Induced MAM Ca2+ Uncoupling and Contractile Dysfunction in an Early Mouse Model of Diabetic HFpEF

Dia

Léon

Chanon

et al. 2022

IJMS

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Diabetic cardiomyopathy (DCM) is a leading complication in type 2 diabetes patients. Recently, we have shown that the reticulum-mitochondria Ca2+ uncoupling is an early and reversible trigger of the cardiac dysfunction in a diet-induced mouse model of DCM. Metformin is a first-line antidiabetic drug with recognized cardioprotective effect in myocardial infarction. Whether metformin could prevent the progression of DCM remains not well understood. We therefore investigated the effect of a chronic 6-week metformin treatment on the reticulum-mitochondria Ca2+ coupling and the cardiac function in our high-fat high-sucrose diet (HFHSD) mouse model of DCM. Although metformin rescued the glycemic regulation in the HFHSD mice, it did not preserve the reticulum-mitochondria Ca2+ coupling either structurally or functionally. Metformin also did not prevent the progression towards cardiac dysfunction, i.e., cardiac hypertrophy and strain dysfunction. In summary, despite its cardioprotective role, metformin is not sufficient to delay the progression to early DCM.

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Section: Discussionmentioning

confidence: 94%

Effect of Metformin on T2D-Induced MAM Ca2+ Uncoupling and Contractile Dysfunction in an Early Mouse Model of Diabetic HFpEF

Dia

Léon

Chanon

et al. 2022

IJMS

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“…The in vitro cells were passaged in high (4.5 g/L) or low (1 g/L) glucose conditions to mimic pathological hyperglycemic and low postprandial-glycemic levels, respectively. Cardiovascular disease is a common diabetic comorbidity [ 16 , 32 – 35 ], therefore murine aorta, ventricle (apex), and atrial heart tissues were compared across non-diabetic control mice and the induced diabetic mouse model.…”

Section: Resultsmentioning

confidence: 99%

Ribonucleosides from tRNA in hyperglycemic mammalian cells and diabetic murine cardiac models

et al. 2023

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“…Hearts exhibit increased interstitial and perivascular fibrosis in both sexes, although there are variable reports on its magnitude. 76 , 77 , 78 Other cardiac features include altered titin isoform expression and/or modifications, 76 , 79 , 80 impaired NO/cGMP/PKG signaling 78 , 79 , 80 and Ca 2+ handling, 76 , 78 increased ER stress, 81 NOS2 expression, 82 and mitochondrial dysfunction. 83 , 84 , 85 Transcriptomic, metabolic, epigenetic, and posttranslational modifications in the db/db model are emerging as fundamentals contributing to the development and progression of diabetes.…”

Section: Conventional Preclinical Modelsmentioning

confidence: 99%

Genomic, Proteomic, and Metabolic Comparisons of Small Animal Models of Heart Failure With Preserved Ejection Fraction: A Tale of Mice, Rats, and Cats

Smith

Altara

Amin

et al. 2022

JAHA

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Heart failure with preserved ejection fraction (HFpEF) remains a medical anomaly that baffles researchers and physicians alike. The overall phenotypical changes of diastolic function and left ventricular hypertrophy observed in HFpEF are definable; however, the metabolic and molecular alterations that ultimately produce these changes are not well established. Comorbidities such as obesity, hypertension, and diabetes, as well as general aging, play crucial roles in its development and progression. Various animal models have recently been developed to better understand the pathophysiological and metabolic developments in HFpEF and to illuminate novel avenues for pharmacotherapy. These models include multi‐hit rodents and feline aortic constriction animals. Recently, genomic, proteomic, and metabolomic approaches have been used to define altered signaling pathways in the heart associated with HFpEF, including those involved in inflammation, cGMP‐related, Ca 2+ handling, mitochondrial respiration, and the unfolded protein response in endoplasmic reticulum stress. This article aims to present an overview of what has been learnt by these studies, focusing mainly on the findings in common while highlighting unresolved issues. The knowledge gained from these research models will not simply be of benefit for treating HFpEF but will undoubtedly provide new insights into the mechanisms by which the heart deals with external stresses and how the processes involved can fail.

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Morphological and functional characterization of diabetic cardiomyopathy in db/db mice following exercise, metformin alone, or combination treatments

Cited by 9 publications

References 23 publications

Effect of Metformin on T2D-Induced MAM Ca2+ Uncoupling and Contractile Dysfunction in an Early Mouse Model of Diabetic HFpEF

Effect of Metformin on T2D-Induced MAM Ca2+ Uncoupling and Contractile Dysfunction in an Early Mouse Model of Diabetic HFpEF

Ribonucleosides from tRNA in hyperglycemic mammalian cells and diabetic murine cardiac models

Genomic, Proteomic, and Metabolic Comparisons of Small Animal Models of Heart Failure With Preserved Ejection Fraction: A Tale of Mice, Rats, and Cats

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