As Catherine says, don't try this at home folks , these people were carefully monitored and a 600 cal diet is extremely low.
but it is very interesting
http://www.springerlink.com/content/68r ... lltext.pdf
First the subjects; type 2 diabetes (age 35– 65 years,
HbA1c 6.5–9.0% [48–75 mmol/mol],
diabetes duration <4 years,
stable BMI 25–45 kg/m2). (
my comment:this would exclude the 'thin' 'type 2s')
None of them were on insulin or had any other problems.
There were 15 subjects, 3 did not comply with the diet and one dropped out for an unrelated medical reason so 11 finished it.
The actual diet was basically liquid based (510 calories) 46.4% carbohydrate, 32.5% protein and 20.1% fat; vitamins, minerals and trace elements; supplemented by 3 portions of non starchy vegetables to make up the remaining 90 calories.
I make that as 59g carb, 45g proten. 11.3g fat + whatever is in the veggies .
The return to normal diet :
At the end of the 8 week intervention participants returned
to normal eating but were provided with information
about portion size and healthy eating.
An OGTT was done 12 weeks after the diet ie at 20 weeks since the start. Of the 11: 1 couldn't do the test for unrelated reasons, 3 had returned to diabetic results (ie above 11mmol after glucose challenge) but the others 'passed' the OGTT.
There are a lot of interesting bits in the results. The fasting glucose dropped after the first week. The C peptide (showing how much insulin is being produced) dropped over the 8 weeks, trigs dropped a lot. The circulating fatty acids rose initially (and the liver function test showed a biref deterioration) but then steadily improved. At 20 weeks these levels had dropped further still.
The authors say
The data are consistent with the
hypothesis that the abnormalities of insulin secretion and
insulin resistance that underlie type 2 diabetes have a
single, common aetiology, i.e. excess lipid accumulation in
the liver and pancreas [11].
There is a lot in the discussion section about the role of fats in the organs and free fatty acids in circulation. There is aso some discussion about the genetic susceptibility to 'pancreatic fat accumulation in terms of inhibition of glucose-dependent insulin secretion.'
There are limitations
1) the numbers involved, though they say the low numbers meant it could be a carefully controlled study and also so that they could use MRI scans to determine liver and pancreatic fat.
2) I t
hink that due to the limltations of MRI scans in measuring the pancreatic fat.
They can't actually look at the fat in the insulin producing islets and that this would be better but animal studies suggest the amount of fat in the islets and pancreas are related.
3)People had only had diabetes diagnosed for a short time. It doesn't necessarily apply to people who have had it for longer. (further studies etc)
4) There needs to be longer follow up after return to normal diet.
Conclusion
This study demonstrates for the first time the time course of a return of normal beta cell function and hepatic glucose output by acute restriction of dietary energy intake in individuals with type 2 diabetes. The changes occurred in association with decreases in pancreatic and liver triacylglycerol concentrations. This new insight allows an understanding of the causality of
type 2 diabetes in individuals as well as in populations. It carries major implications for information to be given to newly diagnosed patients, who should know that they have a potentially reversible condition and not one that is inevitably progressive
.