Type 2 diabetes mellitus (T2DM) represents a worldwide pandemic, with interrelated genetic, metabolic, lifestyle, and environmental factors all contributing to its development [1]. As a common clinical chronic disease, T2DM occurs with metabolic and endocrine disorders [2]. Arteriosclerotic cardiovascular disease (ASCVD) represents the major co-morbidity associated with T2DM and the principal reason for death and disability among patients, thereby creating a huge economic burden [3, 4]. Emerging evidence has indicated that the occurrence of heart failure (HF), the initial manifestation of ASCVD, in patients with diabetes is relatively high [5]. The likelihood of HF in patients with T2DM is 12–57% [6]. Thus, patients with HF are prone to receive worse prognoses than those patients without HF [7]. Type 2 diabetes also represents an independent risk factor of HF since a higher risk of HF is observed in patients suffering from type 2 diabetes [8]. Moreover, the mortality rate of T2DM patients with HF is significantly higher, approximately 11 to 13 times, than those without HF [6]. Obviously, the interaction between type 2 diabetes and HF exists in both occurrence and clinical outcomes. However, the identification of predictors and intervention targets is still required.

Generally, left ventricular hypertrophy (LVH) is the aberrant enlargement of the left ventricular mass due to an increase in cardiomyocyte size, which is modulated by volume and/or pressure overload [9]. In the beginning, physiological LVH is benign and protective, and it regresses when physical activity is reduced or stopped. While pathological LVH is compensative and maladaptive, even evolving toward left ventricular dysfunction and HF [10]. LVH has been indicated as an independent risk factor of HF and it is relatively common in Chinese T2DM patients [11]. In prediabetes, an increase in LV quality can be observed upon impaired glucose tolerance [12]. The left ventricular mass/volume ratio and relative wall thickness are increased in diabetes patients [13]. Thus, it is a representative manifestation of diabetic cardiomyopathy.

Researchers have found that the body mass index (BMI), a well-known measure in daily life, has strong associations with LVH [14]. Vitamin D is a considerable hormone with corresponding receptors in cardiac myocytes, while its deficiency is related to cardiovascular diseases, including LVH. Moreover, parathyroid hormone (PTH) is a predicting variable of LVH, a decrease in which can cause a reduction in left ventricular mass [15]. A positive correlation exists between the left ventricular mass index and fasting blood glucose (FBG) or glycosylated hemoglobin A1c (HbA1c) [16]. In type 2 diabetes and HF patients, high HbA1c is related to an increase in cardiovascular mortality [12]. Insulin sensitivity, C-peptide, homeostasis model assessment index (HOMA-IR), HOMA-$\beta$, and serum creatinine (Cr) are also commonly tested variables in studies on LVH [17, 18, 19]. Thus, in this research, these possible variables were examined to explore potential intervention targets.

This is a retrospective research study, meaning a causality relationship could not be provided between LV and BMI or between LA and BMI.

This study found that 10% of patients with normal ejection fraction values but no clinical symptoms of heart failure had left ventricular volume dilation. Following, the patients with hypertension, coronary heart disease, acute myocardial infarction, and cardiomyopathy were removed, and the influence factors were adjusted. Among the potential influence factors, such as FBG, age, eGFR, and BMI, only BMI was positively related to left ventricular volume in patients with either left ventricular or left atrial enlargement. This is in accordance with the finding that the introduction of novel therapies, such as sodium-glucose co-transporter 2 (SGLT2i) improved the risk of HF in diabetic patients [21]. Moreover, SGLT2i has also been proven to ameliorate cardiac remodeling, previously characterized by the improvement of left ventricular global longitudinal strain (LV-GLS) and myocardial work efficiency in hearts with preserved ejection fraction, while BMI owns a positive correlation with left ventricular size [22], which implies that patients with higher BMIs possess bigger left ventricular volumes and HF risks [23]. Thus, BMI may be an early predictor of HF in type 2 diabetes patients. Moreover, controlling BMI to prevent obesity may be a possible method to prevent left ventricular enlargement and HF in diabetic patients. However, since this study was a retrospective study and data relating to glycosylated hemoglobin was incomplete, performing linear regression analysis was not suitable for analyzing causality. Therefore, further prospective controlled studies are needed to improve and support the above phenomenon.

Previous papers have studied the effect of body weight in diabetic rats. Body weight gain and feed intake were shown to be decreased by fructans in diabetic rats [24]. Insulin can also decrease body weight and food intake in diabetic rats [25]. The body weight of diabetic rats treated by gastrectomy is significantly lower than in sham-operated diabetic rats [26]. Body weight is a common symptom in diabetic rats, which is generally recognized as a testing index. We also observed that increases in weight in diabetic rats caused sharp increases in heart weight, the transverse and longitudinal diameters of the heart, the number of fibroblasts, and the expression of collagen IV in cardiomyocytes. Consistent with the results of population studies, increases in body weight accelerated pathological changes in the myocardium and aggravated LVH in diabetic rats.

It has already been reported that inflammatory reactions are a mechanism that leads to LVH [27]. The accumulation of globotriaosylceramide induces LVH by releasing pro-inflammatory cytokines and growth-promoting factors as well as inducing oxidative stress [28]. In renovascular hypertensive rats, treatment of olmesartan mitigates LVH and reduces IL-6 levels [28]. One research study investigated the function of inflammation in epicardial adipose tissue in heart diseases [29]. Accumulating data suggest that type 2 diabetic patients present with hyperglycemia and metabolic disorders, such as lipid metabolism and protein metabolism disorders [30, 31]. It is not a simple disease but a series of syndromes of multiple organs caused by metabolic disorders [32]. Insulin resistance exerts a vital role in the development of type 2 diabetes, which is closely related to BMI augmentation [33]. For patients with type 2 diabetes, BMI is of great significance to left ventricular volume dilation and increases in HF risk, not only in the heart but also in highlighting the importance of weight management in metabolic balance. Although some research showed that obesity may have an influence on vascular aging and arterial stiffness [34, 35], the subjects we included had mostly normal BMI or were overweight, and only in a few cases, were they diagnosed as obese.

It is indicated from a study that in patients suffering from type 2 diabetes, BMI is an independent risk for LVH [36]. Additionally, a positive correlation of body weight with heart size in type 2 diabetic rats was observed [37]. These data hint that body weight is a possible independent risk for LVH in type 2 diabetic patients. In the subsequent exploration of the in-depth mechanisms involved, we detected that the follow-up weight and the content of myocardial inflammatory factors in rats were markedly increased, and that pyroptosis existed in pericardial adipocytes. It has been proposed that the inflammatory response is a pathogenesis that accounts for the complications associated with type 2 diabetes [38].

As far as the literature we retrieved, no previous research has been conducted on the etiology and mechanism of left ventricular volume dilation and HF in patients with type 2 diabetes. This work provides new ideas for the early prevention of left ventricular volume dilation, HF, and ASCVD in type 2 diabetic patients.

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

JZ, ZY, XF, QF, and YX conceptualized and designed the study. JZ and ZY were responsible for data acquisition and preliminary analysis, while XF and QF conducted further analysis and interpretation of the data. ZY, XF were involved in the visualisation of the data, and ZY, XF, QF, and YX were all responsible for writing parts of the manuscript. JZ, as the corresponding author, provided comprehensive oversight of the research design and data analysis, and played a leading role in drafting and critically reviewing the manuscript. YX provided important technical support and insights. All authors edited and revised the manuscript to ensure accuracy and completeness of content. All authors have read and approved the final manuscript. Each author has fully participated in the work and agreed to be accountable for all aspects of the work, ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

The ethics of this study was approved by the Human Research Ethics Committee of Ningbo Huamei Hospital, Chinese Academy of Sciences (Ningbo No.2 hospital) (Ethics No.: YJ-KYSB-NBEY-2019-158-01). This study was retrospective and did not require informed consent from the patients.

Not applicable.

The authors acknowledge all the participants in this study. This study supported by Key projects of natural fund of Ningbo in 2020 (Grant No. 202003N4021), the Medical Scientific Research Foundation of Zhejiang Province, China (Grant No. 2020RC105), the research Foundation of Hwa Mei Hospital, University of Chinese Academy of Sciences, China (Grant No. 2020HMKY05) and the Project of NINGBO Leading Medical & Health Discipline (Grant No. Number: 2022-F18).

The authors declare no conflict of interest.