A “Cure” for Type 2 Diabetes

In case you haven’t already heard, researchers are now reporting that Type 2 Diabetes may (possibly) be reversed by a restricted low-calorie diet:

Adhering to the strict 600 calorie-a-day diet causes fat levels in the pancreas to plummet, restoring normal function, found Prof Roy Taylor of Newcastle University.

The discovery, a “radical change” in understanding of the condition, holds out the possibility that sufferers could cure themselves – if they have the willpower.

Until recently received medical wisdom was that Type 2 diabetes was largely irreversible.

But this small-scale study indicates that defeating it could be easier than commonly thought.

Prof Taylor asked 11 volunteers, all recently diagnosed, to go on what he admitted was an “extreme diet” of specially formulated drinks and non-starchy vegetables, for eight weeks.

Hyscience comments:

As the article goes on to point out, the trial study involved only 11 patients that ate a “meal-replacement” milkshake of 150 calories three times a day. This was supplemented with three portions of non-starchy vegetables including cabbage, broccoli, peppers, tomatoes, cucumber and lettuce. After one week, their pre-breakfast blood sugar levels had returned to normal and an MRI scan revealed that the fat levels in the pancreas were also normal, down from around eight per cent to six per cent.

Notes to self:

  • Great news – perhaps (I think)
  • “small-scale study” –  The smaller the study the less likely the results will be supported over time, esp. considering all of the potential influential factors.  Something like 33% of all reported major medical studies is contradicted within five years.
  • Radical change in management – pharma and device companies may need to revisit their strategic roadmap if this research is supported by larger scale studies

 

Type 2 Diabetes – an autoimmune disease

Type 2 diabetes is in the process of being redefined as an autoimmune disease rather than just a metabolic disorder.

A recent study, appearing in Nature Magazine, showed that an antibody called anti-CD20, which targets and eliminates mature B cells in the immune system, stopped diabetes type 2 developing in lab mice prone to develop the disease, and restored their blood sugar level to normal:

Chronic inflammation characterized by T cell and macrophage infiltration of visceral adipose tissue (VAT) is a hallmark of obesity-associated insulin resistance and glucose intolerance. Here we show a fundamental pathogenic role for B cells in the development of these metabolic abnormalities. B cells accumulate in VAT in diet-induced obese (DIO) mice, and DIO mice lacking B cells are protected from disease despite weight gain. B cell effects on glucose metabolism are mechanistically linked to the activation of proinflammatory macrophages and T cells and to the production of pathogenic IgG antibodies. Treatment with a B cell–depleting CD20 antibody attenuates disease, whereas transfer of IgG from DIO mice rapidly induces insulin resistance and glucose intolerance. Moreover, insulin resistance in obese humans is associated with a unique profile of IgG autoantibodies. These results establish the importance of B cells and adaptive immunity in insulin resistance and suggest new diagnostic and therapeutic modalities for managing the disease.

One of the many reasons that this is significant is that it could lead to future novel treatments.