Figure 1 (31):
Blood glucose levels remain stable in a healthy individual, regulated at 4-7.8 mmol/L (33) Insulin stimulates many intracellular pathways, including enhanced production of triglycerides. These leave hepatocytes in very low density lipoproteins (VLDL) and are stored in visceral adipocytes via insulin’s activation of lipoprotein lipase. Increased visceral fat and VLDLs lead to β-cell dysfunction and insulin resistance (25) (13) (29)(19)(17).

Pancreatic triglycerides in T2DM are associated with the condition, rather than decreased body fat (19). This was due to T2DM patients showing a substantial decrease in pancreatic triglycerides compared to those without T2DM, when both groups had undergone substantial weight loss. VLDLs transport fats to extra-hepatic cells and tissues (fig1), these decreased by 20%. It is suggested that this accounted for the fall in pancreatic fat. A loss in total pancreatic fat has been shown to mediate a return to β-cell function (17). This is a suggested mechanism of T2DM remission in responding patients. These patients recorded higher levels of insulin secretion at baseline. Those that recorded low levels of insulin secretion at baseline couldn’t regain β-cell function.

In the Steven et al. study all medication was discontinued and all participants followed the same diet. Also, it featured a greater scope of diabetic patients (including >10 years). However, fasting glucose levels after treatment positively correlated with the duration of T2DM in participants  (19).

Both initial phases of each study were inherently ketogenic, delivering 600-800kj with a maximum of 50% carbohydrate. However, the Goday et al. study delivered 1-1.6 g/kg/d protein which has been shown to have positive implications for adherence due to increased satiety, lower energy expenditure (by sparring fat free mass), improved body composition and prevention of weight cycling (20). In the Steven et al. study, participants found it difficult readjusting to normal eating. Perhaps therefore, a macronutrient mix of higher proteins and fats could improve a transition to eating.

In other studies, regaining glucose control was shown to be more efficacious in ketogenic diets compared to LC diets (15). Enhanced ketosis is associated with higher urinary ketones and increased glycaemic control in non-insulin dependent patients with T2DM (15). There was no difference in weight loss. This means that glycaemic control was independent of overall weight loss. This further provides support that a ketogenic low calorie diet is a robust treatment of reversal of T2DM through the mobilisation of visceral fat. Several studies show that visceral fat in patients with T2DM is independent of overall obesity; based on the theory of a ‘personal fat threshold’ (6). Non-obese patients with T2DM still respond to the same diet and reverse T2DM (6).

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