To date, the association of dietary salt intake with the glycaemia response of T2D was not well investigated and understood in China, in T2D patients in particular. The present study, using clinical data of the outpatient department of the Endocrinology and MMC, was to analyze the association of dietary salt and the glycaemia response of T2D (plasma glucose, insulin and HbA1c) in T2D patients in Ningbo. The findings indicated that higher dietary salt was positively associated with increasing FPG and HbA1c.
One previous study conducted on Ningbo healthy residents in Ningbo showed that higher fasting blood glucose level was found in the group of higher dietary salt intake (≥ 6g/d) compared to it in the group of dietary salt (< 6g/d). 12 The results of the Chinese study are in line with our findings on FPG among Chinese in Ningbo, although target populations are different. The mechanism of the association between dietary salt and the glycaemia response in T2D patients is unclear yet. Increasing dietary salt intake may suppress activities of the renin-angiotensin-aldosterone system 18 19 and staminate sympathetic activity 20 and cause insulin resistance. 21 22 Therefore, it may contribute to the development and progression of T2D complications.
The majority studies on the relationship between dietary salt and the glycaemia response of T2D have been explored through observational studies, intervention studies and meta-analysis among healthy population. 12 23 24 However, few studies have been conducted on T2D patients. Our findings showed that dietary salt was positively associated with HbA1c, which is consistent with the results from one randomized controlled trial (RCT) on salt reduction. 24 This observer-blind RCT recruiting 70 patients with acute non-cardio-embolic mild ischemic stroke reported that HbA1c decreased more in the lifestyle intervention group providing reduction in salt intake compared to controlled group, although no significant difference was found between 2 groups. 24 Likewise, Strazzullo and his colleagues conducting a meta-analysis including 13 studies with 177025 participants indicated an effect between the HbA1c level and dietary sodium for the development of CVD. 25
Higher dietary salt was found to be related to high prevalence of overweight and obesity compared to lower dietary salt in the present study. Additionally, high blood lipid levels were significantly related to increasing dietary salt intake in our study. The potential hypothesis is that high dietary salt might increase plasma glucose and postprandial plasma glucose in T2D patients through weight gain due to appetite and over-consumption of energy, fat and cholesterol. 26 Eventually, increased fat free acid level in blood can inhibit insulin suppression of hepatic glucose production. 27 Dietary salt is a key factor to increase the feeling of thirsty, resulting in more amount of fluid drinks. 28 Increasing 1 g/d dietary salt intake was positively associated with an increase in 100 g/d total fluid and 27 g/d sugar-sweetened soft drink consumption. 29 Hereby, it may contribute to high blood pressure/hypertension.
Several dietary guidelines recommend and advocate that patients with T2D should decrease their dietary salt intake due to benefits for lowing a modest blood pressure. 89 In the present study, the results derived from description analysis showed that no significant difference in SBP and DBP was found across dietary salt categories. The WHO Cardiovascular Diseases and Alimentary Comparison (WHO-CARDIAC) Study conducted on pre- and post-menopausal women from 17 countries and reported that 24 h sodium excretion was positively associated with blood pressure. 30 In T2D patients, hypertension is associated with a range of adverse outcomes for further developing cardiovascular disease and premature mortality. 31 The different result in our study might be attributed to the nature of cross-sectional study design.
Interestingly, dietary salt was not found to be significantly associated with postprandial plasma glucose and postprandial insulin. Few studies have been investigated on the relationship between dietary salt, and postprandial plasma glucose and insulin responses in T2D patients. An intervention study including six healthy adults, assigned randomly meals with or without added salt, suggested that moderate dietary salt intake increased postprandial plasma glucose and insulin levels. 23 Sodium can facilitate the absorption of glucose in the small intestine. 32 The potential reason can be that most of our participants had been diagnosed with T2D for a certain period so that postprandial plasma glucose and insulin responses to dietary salt cannot be the same like healthy participants due to insensitive digestion system.
The relationship between dietary salt intake and hypertension has been well understood in Chinese population. In addition, the knowledge on glycaemia control through the duration and the quantity of carbohydrate consumption from foods is understood as well. 33 Patients with diabetes are recommended to restrict total consumption of energy and carbohydrates in order to control body weight and blood glucose levels. However, the knowledge of the effect of dietary salt intake on the glycaemia response in T2D patients needs to get more attention. Therefore, hospital-based education and community-based education are necessarily required regarding health effects of excess salt intake, food labelling and food sources.
This is the first study on the association between dietary salt intake and the glycaemia response in T2D patients in Ningbo with standard national management and treatment by MMC. Nevertheless, several study limitations need to be considered. First, causality between dietary salt intake and factors of T2D cannot be achieved according to the nature of cross-sectional study design. Second, because of the structure of FFQ, quantitative dietary salt intake could not be obtained, although the categories of salt intake could be collected from the patients. Therefore, it may not accurately reflect daily dietary salt intake among T2D patients. Third, total energy intake was not adjusted in the model due to FFQ. Additionally, the reported dietary salt level could be biased towards misreporting because of patients’ psychology. Furthermore, due to patients from Eastern China, so the findings cannot be representative for the entire Chinese population with T2D.