Does Vitamin C reduce plasma glucose?

Increased oxidative stress appears to be a significant factor leading to insulin resistance, dyslipidaemia, β-cell dysfunction, impaired glucose tolerance and ultimately leading to type 2 diabetes (T2D). Ascorbic acid (AA) is a water soluble anti-oxidant that reduces oxidative damage at the cellular and tissue level. So, logically, AA supplementation should therefore reduce oxidate stress and lead to improvement in glycaemic control in patients with diabetes. Does it?

Logically, if you reduce oxidative stress, insulin sensitivity should improve. However, randomised control trials exploring whether AA improves glycaemic control have mixed findings. (1-4). Ashor AW et al conducted a systematic review and meta-analysis of the RCTs (5). Overall, AA did not modify glucose, HbA1c and insulin concentrations. However, in subgroup analysis, they did find AA improved glucose concentrations in patients with T2D, older individuals and if given for more than 30 days. AA had greater effects on fasting than post prandial glucose.

The latest study looking at the effect of AA on glycaemic control is an Australian study published in the Diabetes, Obesity and Metabolism this week (6). It is a randomised, cross over trial in individuals with T2D. 27 patients on oral therapy or diet were randomised to received either 500mg of ascorbic acid or placebo. Continuous glucose monitoring was used for 48 hours to monitor the post prandial glucose for 3.5 hours post prandial for the three meals. The cumulative total of 10.5 hours were compared between the groups.

Over the study period of 4 months, daily 10.5-hour postprandial glucose decreased by 36% (P < 0.01) during AA supplementation. The mean post prandial glucose was reduced by 1.1 mmol/L with AA supplementation. The duration of day spent with hyperglycaemia (>10.0 mmol/L) also significantly decrease by 2.8 hours per day with AA supplementation. The average 24-hour glucose also significantly decreased with AA supplementation but only by 0.8mmol/L. However, the HbA1c, fasting glucose and fasting insulin did not differ between the groups.

Systolic and diastolic pressure were also significantly reduced by 7mm and 5mm Hg respectively. Body composition, lipids, energy expenditure and renal and liver function were not affected by AA supplementation.

The effects of AA on glycaemic control in patients with T2D seems very impressive but is the effect clinically significant? The reduction in post prandial glucose did translate to a reduction in time with hyperglycaemia. This have potential clinical importance given that post-prandial hyperglycaemia has been considered an independent risk factor for cardiovascular disease and cardiovascular events in individuals with T2D.(7-9).

Previous studies that reported significant improvements in HbA1c after AA supplementation included more participants, enrolled participants with a higher baseline HbA1c and/or undertook AA supplementation for a longer period (10–13). Perhaps, HbA1c may be improved with a more prolonged supplementation period.

AA is an antioxidant and it is thought that the anti-oxidant effect may have decreased the oxidative stress on muscles which leads to improved peripheral glucose disposal.  Perhaps, patients with T2D have a greater need for AA. Indeed, patients with T2D have been found to have lower plasma Vitamin C concentrations compared with subjects with normal glucose tolerance (14-16). There are several proposed mechanisms including:

(1) increased ascorbate excretion in those with microalbuminuria,

(2) blood glucose may compete with vitamin C for uptake into cells due to its structural similarity to the oxidised form (dehydroascorbic acid), and

(3) increased oxidative stress may deplete antioxidant stores.

AA could be useful as an adjunct in patients with T2D for better control of glucose but the clinical significance is uncertain.

Access the latest study here.


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