Article first published as Drastic Calorie Restriction may Reverse Type II Diabetics to Normal on Technorati.
Type II diabetes mellitus is due to the combined effect of pancreatic beta cell failure to produce insulin in response to diet and peripheral tissue resistance to insulin. Most of the research point to the fact that the problem is due to direct toxicity of fat on liver and pancreas.
After gastric bypass surgery for obese, their insulin sensitivity improved as well as the pancreatic beta cell function. In gastric bypass operation there is severe negative energy balance.
It
was thought that restricting calorie to a larger extent may also have
similar effect on obese diabetics. Normally, an adult male is advised
for intake of around 2000 calories per day. The experiment began by
restricting calorie intake to 600 calories per day.
This was first tested on eleven recently diagnosed type II diabetic patients in UK. The doctors restricted their diet for 12 weeks and found that they no longer need drugs for diabetes. This was first reported in the Diabetologia and widely reported in the media .
The individuals with type 2 diabetes were given a liquid diet formula (46.4% carbohydrate, 32.5% protein and 20.1% fat; vitamins, minerals and trace elements; 510 kcal/day). This was supplemented with three portions of non-starchy vegetables such that total energy intake was about 2.5 MJ (600 kcal)/day. Participants were provided with suggestions of vegetable recipes to enhance compliance by varying daily eating.
They were also advised to drink at least 2 l of water or other energy-free beverages each day, and asked to maintain their habitual level of physical activity. At the end of the 8 week intervention participants returned to normal eating, but were provided with information about portion size and healthy eating.
This study demonstrates that the twin defects of beta cell failure and insulin resistance that underlie type 2 diabetes can be reversed by acute negative energy balance alone.
A hierarchy of response was observed, with a very early change in hepatic insulin sensitivity and a slower change in beta cell function. In the first 7 days of the reduced energy intake, fasting blood glucose and hepatic insulin sensitivity fell to normal, and intra-hepatic lipid decreased by 30%.
Over the 8 weeks of dietary energy restriction, beta cell function increased towards normal and pancreatic fat decreased. Following the intervention, participants gained 3.1±1.0 kg body weight over 12 weeks, but their HbA1c (Glycated Haemoglobin) remained steady while the fat content of both pancreas and liver did not increase.
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.
According to another research presented at the International Diabetes Federation World Diabetes Congress 2011, “Beta cell function can improve after just 12 weeks of weight loss in patients with type 2 diabetes”. (International Diabetes Federation (IDF) World Diabetes Congress 2011. Abstract O-0473. Presented December 5, 2011)
For the first time, these changes have been shown to correlate with a decrease in pancreatic polypeptide, reported Hana Kahleova, MD, from the diabetes centre at the Institute for Clinical and Experimental Medicine in Prague, Czech Republic.
This study involved 74 subjects with type 2 diabetes who were being treated with oral hypoglycemic agents. Mean age was 56.6 years, mean body mass index was 35.8 kg/m², and mean glycated haemoglobin level was 7.7%.
Subjects were prescribed 12 weeks of a weight-loss diet alone (a reduction of 500 kcal/day) followed by 12 weeks of the same diet but with aerobic exercise added.
At baseline, 12 weeks, and 24 weeks, insulin sensitivity, plasma concentration of gastrointestinal peptides and beta cell function were assessed, as well as the insulin secretory rate was calculated by C-peptide deconvolution.
In the cohort, mean weight loss was 5.0kg (P = .001) after 12 weeks of dietary intervention; weight did not change significantly after the addition of exercise.
Both fasting and stimulated plasma glucose and insulin concentrations decreased in response to the diet. In the case of glucose, there was no change after the addition of exercise, but plasma insulin decreased further with exercise.
Similarly, plasma concentrations of C-peptide decreased in response to the diet and further in response to exercise.
In addition, peripheral insulin sensitivity and insulin secretion increased, and glucose sensitivity of beta cells increased by 26% in response to the diet without a significant change after the addition of exercise.
They also observed a marked decrease in both fasting and hyperinsulinemic concentrations of pancreatic polypeptide in response to dietary intervention. There was no significant change in other gastrointestinal peptides.
Pancreatic polypeptide is a novel marker, and a reduction in pancreatic polypeptide correlated with an improvement in beta cell function.
Beta cell function is really an issue in type2 diabetes in terms of the natural history and progression of the disease.
Perhaps more research in this line will go a long way in reversing our thinking, “Diabetic status cannot be reversed”; and the hopelessly unthinkable can be achieved.
Type II diabetes mellitus is due to the combined effect of pancreatic beta cell failure to produce insulin in response to diet and peripheral tissue resistance to insulin. Most of the research point to the fact that the problem is due to direct toxicity of fat on liver and pancreas.
After gastric bypass surgery for obese, their insulin sensitivity improved as well as the pancreatic beta cell function. In gastric bypass operation there is severe negative energy balance.
It
was thought that restricting calorie to a larger extent may also have
similar effect on obese diabetics. Normally, an adult male is advised
for intake of around 2000 calories per day. The experiment began by
restricting calorie intake to 600 calories per day. This was first tested on eleven recently diagnosed type II diabetic patients in UK. The doctors restricted their diet for 12 weeks and found that they no longer need drugs for diabetes. This was first reported in the Diabetologia and widely reported in the media .
The individuals with type 2 diabetes were given a liquid diet formula (46.4% carbohydrate, 32.5% protein and 20.1% fat; vitamins, minerals and trace elements; 510 kcal/day). This was supplemented with three portions of non-starchy vegetables such that total energy intake was about 2.5 MJ (600 kcal)/day. Participants were provided with suggestions of vegetable recipes to enhance compliance by varying daily eating.
They were also advised to drink at least 2 l of water or other energy-free beverages each day, and asked to maintain their habitual level of physical activity. At the end of the 8 week intervention participants returned to normal eating, but were provided with information about portion size and healthy eating.
This study demonstrates that the twin defects of beta cell failure and insulin resistance that underlie type 2 diabetes can be reversed by acute negative energy balance alone.
A hierarchy of response was observed, with a very early change in hepatic insulin sensitivity and a slower change in beta cell function. In the first 7 days of the reduced energy intake, fasting blood glucose and hepatic insulin sensitivity fell to normal, and intra-hepatic lipid decreased by 30%.
Over the 8 weeks of dietary energy restriction, beta cell function increased towards normal and pancreatic fat decreased. Following the intervention, participants gained 3.1±1.0 kg body weight over 12 weeks, but their HbA1c (Glycated Haemoglobin) remained steady while the fat content of both pancreas and liver did not increase.
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.
According to another research presented at the International Diabetes Federation World Diabetes Congress 2011, “Beta cell function can improve after just 12 weeks of weight loss in patients with type 2 diabetes”. (International Diabetes Federation (IDF) World Diabetes Congress 2011. Abstract O-0473. Presented December 5, 2011)
For the first time, these changes have been shown to correlate with a decrease in pancreatic polypeptide, reported Hana Kahleova, MD, from the diabetes centre at the Institute for Clinical and Experimental Medicine in Prague, Czech Republic.
This study involved 74 subjects with type 2 diabetes who were being treated with oral hypoglycemic agents. Mean age was 56.6 years, mean body mass index was 35.8 kg/m², and mean glycated haemoglobin level was 7.7%.
Subjects were prescribed 12 weeks of a weight-loss diet alone (a reduction of 500 kcal/day) followed by 12 weeks of the same diet but with aerobic exercise added.
At baseline, 12 weeks, and 24 weeks, insulin sensitivity, plasma concentration of gastrointestinal peptides and beta cell function were assessed, as well as the insulin secretory rate was calculated by C-peptide deconvolution.
In the cohort, mean weight loss was 5.0kg (P = .001) after 12 weeks of dietary intervention; weight did not change significantly after the addition of exercise.
Both fasting and stimulated plasma glucose and insulin concentrations decreased in response to the diet. In the case of glucose, there was no change after the addition of exercise, but plasma insulin decreased further with exercise.
Similarly, plasma concentrations of C-peptide decreased in response to the diet and further in response to exercise.
In addition, peripheral insulin sensitivity and insulin secretion increased, and glucose sensitivity of beta cells increased by 26% in response to the diet without a significant change after the addition of exercise.
They also observed a marked decrease in both fasting and hyperinsulinemic concentrations of pancreatic polypeptide in response to dietary intervention. There was no significant change in other gastrointestinal peptides.
Pancreatic polypeptide is a novel marker, and a reduction in pancreatic polypeptide correlated with an improvement in beta cell function.
Beta cell function is really an issue in type2 diabetes in terms of the natural history and progression of the disease.
Perhaps more research in this line will go a long way in reversing our thinking, “Diabetic status cannot be reversed”; and the hopelessly unthinkable can be achieved.
