Australian researchers say fat is 'sixth taste'
March 8, 2010
It's a theory set to confirm why humans are so fond of fatty foods such as chips and chocolate cake: in addition to the five tastes already identified lurks another detectable by the palate -- fat.
"We know that the human tongue can detect five tastes -- sweet, salty, sour, bitter and umami (a savoury, protein-rich taste contained in foods such as soy sauce and chicken stock)," Russell Keast, from Deakin University, said Monday.
"Through our study we can conclude that humans have a sixth taste -- fat."
Researchers tested 30 people's ability to taste a range of fatty acids in otherwise plain solutions and found that all were able to determine the taste -- though some required higher concentrations than others.
They then developed a screening test to see how sensitive people were to the taste and found that, of the 50 people tested, their ability to detect fat was linked to their weight -- a finding which could help counter obesity.
"We found that the people who were sensitive to fat, who could taste very low concentrations, actually consumed less fat than the people who were insensitive," Keast told AFP.
"We also found that they had lower BMIs (Body Mass Indexes)."
Keast said the research, conducted in collaboration with the University of Adelaide, New Zealand's Massey University and Australian science body CSIRO, suggested that the taste of fat could trigger a mechanism in the body.
"We all like eating fatty foods. What we speculate is (that) the mechanism is to do with stopping eating. Your body is able to tell you you've had enough and stop," he explained.
"And if you are insensitive to it, you're not getting that feedback."
With fats easily accessible and commonly consumed, it was possible that people may become desensitised to the taste of fat, leaving some more prone to overindulging in calorie-rich foods, he added.
The results, published in the British Journal of Nutrition, have not definitively classified fat as a taste but Keast says the evidence is strong and mounting.
For something to be classified as a taste there needed to be proven receptor mechanisms on taste cells in the mouth, he said.
"We have what... we will call possible candidate receptors for fat on taste receptor cells," he said.
Thursday, 27 October 2011
Study Shows Why It’s Hard to Keep Weight Off By GINA KOLATA Published: October 26, 2011
For years, studies of obesity have found that soon after fat people lost weight, their metabolism slowed and they experienced hormonal changes that increased their appetites. Scientists hypothesized that these biological changes could explain why most obese dieters quickly gained back much of what they had so painfully lost.
GETTY IMAGES
But now a group of Australian researchers have taken those investigations a step further to see if the changes persist over a longer time frame. They recruited healthy people who were either overweight or obese and put them on a highly restricted diet that led them to lose at least 10 percent of their body weight. They then kept them on a diet to maintain that weight loss. A year later, the researchers found that the participants’ metabolism and hormone levels had not returned to the levels before the study started.
The study, being published Thursday in The New England Journal of Medicine, is small and far from perfect, but confirms their convictions about why it is so hard to lose weight and keep it off, say obesity researchers who were not involved the study.
They cautioned that the study had only 50 subjects, and 16 of them quit or did not lose the required 10 percent of body weight. And while the hormones studied have a logical connection with weight gain, the researchers did not show that the hormones were causing the subjects to gain back their weight.
Nonetheless, said Dr. Rudolph Leibel, an obesity researcher at Columbia, while it is no surprise that hormone levels changed shortly after the participants lost weight, “what is impressive is that these changes don’t go away.”
Dr. Stephen Bloom, an obesity researcher at Hammersmith Hospital in London, said the study needed to be repeated under more rigorous conditions, but added, “It is showing something I believe in deeply — it is very hard to lose weight.” And the reason, he said, is that “your hormones work against you.”
In the study, Joseph Proietto and his colleagues at the University of Melbourne recruited people who weighed an average of 209 pounds. At the start of the study, his team measured the participants’ hormone levels and assessed their hunger and appetites after they ate a boiled egg, toast, margarine, orange juice and crackers for breakfast. The dieters then spent 10 weeks on a very low calorie regimen of 500 to 550 calories a day intended to makes them lose 10 percent of their body weight. In fact, their weight loss averaged 14 percent, or 29 pounds. As expected, their hormone levels changed in a way that increased their appetites, and indeed they were hungrier than when they started the study.
They were then given diets intended to maintain their weight loss. A year after the subjects had lost the weight, the researchers repeated their measurements. The subjects were gaining the weight back despite the maintenance diet — on average, gaining back half of what they had lost — and the hormone levels offered a possible explanation.
One hormone, leptin, which tells the brain how much body fat is present, fell by two-thirds immediately after the subjects lost weight. When leptin falls, appetite increases and metabolism slows. A year after the weight loss diet, leptin levels were still one-third lower than they were at the start of the study, and leptin levels increased as subjects regained their weight.
Other hormones that stimulate hunger, in particular ghrelin, whose levels increased, and peptide YY, whose levels decreased, were also changed a year later in a way that made the subjects’ appetites stronger than at the start of the study.
The results show, once again, Dr. Leibel said, that losing weight “is not a neutral event,” and that it is no accident that more than 90 percent of people who lose a lot of weight gain it back. “You are putting your body into a circumstance it will resist,” he said. “You are, in a sense, more metabolically normal when you are at a higher body weight.”
A solution might be to restore hormones to normal levels by giving drugs after dieters lose weight. But it is also possible, said Dr. Jules Hirsch of Rockefeller University, that researchers just do not know enough about obesity to prescribe solutions.
One thing is clear, he said: “A vast effort to persuade the public to change its habits just hasn’t prevented or cured obesity.”
“We need more knowledge,” Dr. Hirsch said. “Condemning the public for their uncontrollable hedonism and the food industry for its inequities just doesn’t seem to be turning the tide.”
GETTY IMAGES
But now a group of Australian researchers have taken those investigations a step further to see if the changes persist over a longer time frame. They recruited healthy people who were either overweight or obese and put them on a highly restricted diet that led them to lose at least 10 percent of their body weight. They then kept them on a diet to maintain that weight loss. A year later, the researchers found that the participants’ metabolism and hormone levels had not returned to the levels before the study started.
The study, being published Thursday in The New England Journal of Medicine, is small and far from perfect, but confirms their convictions about why it is so hard to lose weight and keep it off, say obesity researchers who were not involved the study.
They cautioned that the study had only 50 subjects, and 16 of them quit or did not lose the required 10 percent of body weight. And while the hormones studied have a logical connection with weight gain, the researchers did not show that the hormones were causing the subjects to gain back their weight.
Nonetheless, said Dr. Rudolph Leibel, an obesity researcher at Columbia, while it is no surprise that hormone levels changed shortly after the participants lost weight, “what is impressive is that these changes don’t go away.”
Dr. Stephen Bloom, an obesity researcher at Hammersmith Hospital in London, said the study needed to be repeated under more rigorous conditions, but added, “It is showing something I believe in deeply — it is very hard to lose weight.” And the reason, he said, is that “your hormones work against you.”
In the study, Joseph Proietto and his colleagues at the University of Melbourne recruited people who weighed an average of 209 pounds. At the start of the study, his team measured the participants’ hormone levels and assessed their hunger and appetites after they ate a boiled egg, toast, margarine, orange juice and crackers for breakfast. The dieters then spent 10 weeks on a very low calorie regimen of 500 to 550 calories a day intended to makes them lose 10 percent of their body weight. In fact, their weight loss averaged 14 percent, or 29 pounds. As expected, their hormone levels changed in a way that increased their appetites, and indeed they were hungrier than when they started the study.
They were then given diets intended to maintain their weight loss. A year after the subjects had lost the weight, the researchers repeated their measurements. The subjects were gaining the weight back despite the maintenance diet — on average, gaining back half of what they had lost — and the hormone levels offered a possible explanation.
One hormone, leptin, which tells the brain how much body fat is present, fell by two-thirds immediately after the subjects lost weight. When leptin falls, appetite increases and metabolism slows. A year after the weight loss diet, leptin levels were still one-third lower than they were at the start of the study, and leptin levels increased as subjects regained their weight.
Other hormones that stimulate hunger, in particular ghrelin, whose levels increased, and peptide YY, whose levels decreased, were also changed a year later in a way that made the subjects’ appetites stronger than at the start of the study.
The results show, once again, Dr. Leibel said, that losing weight “is not a neutral event,” and that it is no accident that more than 90 percent of people who lose a lot of weight gain it back. “You are putting your body into a circumstance it will resist,” he said. “You are, in a sense, more metabolically normal when you are at a higher body weight.”
A solution might be to restore hormones to normal levels by giving drugs after dieters lose weight. But it is also possible, said Dr. Jules Hirsch of Rockefeller University, that researchers just do not know enough about obesity to prescribe solutions.
One thing is clear, he said: “A vast effort to persuade the public to change its habits just hasn’t prevented or cured obesity.”
“We need more knowledge,” Dr. Hirsch said. “Condemning the public for their uncontrollable hedonism and the food industry for its inequities just doesn’t seem to be turning the tide.”
Tuesday, 11 October 2011
Pancreatic Cancer, Diabetes Education, Vitamins, Obesity decreasing..Medical News of Interest this week
Summary of some Health News of Interest
Diabetes Education and Cognitive Change Counseling can bring about a reduction in Blood Glucose in patients struggling to control their Diabetes. Some of the reductions are equal to or better than some of the newer medications for Type 2 Diabetes.
More is not Better, a study among older women in Iowa concludes about Vitamin usage and increased mortality.
Multivitamins, Folate, Iron, Magnesium and Zinc seems to be the culprits with worse results with Iron when used without a medical reason to do so. Calcium is protective and Vitamin D is recommended for people with deficiency in Vitamin D.
Three personalities who died in the past few days all died of Pancreatic Cancer: Steve Jobs, The Nobel Prize winner in Medicine from Rockefeller U and Roger Williams the Pianist. Is there an increase in Pancreatic Cancer? Yes there is, especially in people with lifestyle pattern consistent with Ill health. Steve Jobs’ pancreatic cancer was a rare one.
One in eight, approximately, medical advances touted as bringing benefit to humanity are later withdrawn because of the wrong premises on which the studies were based. Do not be the first one to adopt a study nor be the last one to do so, is a good advice given to me at University of Miami School of Medicine.
Now the Good News is: Americans are tad less Overweight than just one year ago, now 36.6 per cent are of normal weight, one per cent higher than one year ago.
Have we succeeded in getting the message across about nutrition and exercise? Don't be so eager to accept the accolades before you realize that a sagging economy have made more people eat at home.
The take home lesson is EATING OUT IN AMERICA is dangerous to an ordinary American!
The results are in for the Science and Maths scores from around the world, the first two cities whose students came out ahead are…
Both in China
Shanghai and Hong Kong. They both recruit their teachers from the top 30 per cent of the graduate cohorts whereas in the countries in the failing grade recruits teachers from the bottom 30 per cent.
Needless to say this will have some implications on the quality of education of future health care providers. But USA is ahead of Asian 2 dollar Wal-Mart manufacturers and 1 800 Foreign Accents from India in that it is still possible to get a good all round education in the USA and not just a career oriented limited education. Hurrah for that!
Some other good news, which we in the Indian Health Services would recognize, is the value of expressive writing. Indians being much more visual people use Talking Circles in which emotions are expressed freely and openly find good results from this ritual which has also symbolic significance in their historic annals.
Dr Pennebaker from UT in Austin, a psychologist has conducted some experiments and he has concluded”
Stress, trauma, and unexpected life developments — such as a cancer diagnosis, a car accident, or a layoff — can throw people off stride emotionally and mentally. Writing about thoughts and feelings that arise from a traumatic or stressful life experience — called expressive writing — may help some people cope with the emotional fallout of such events. But it’s not a cure-all, and it won’t work for everyone. Expressive writing appears to be more effective for people who are not also struggling with ongoing or severe mental health challenges, such as major depression or post-traumatic stress disorder.
I have to admit that Talking Circle is good for people who are suffering from emotional disturbances in addition to their physical problems, such as the PTSD or depression.
Today I was sitting down to a lunch of Alaskan Haddock in Olive oil sprinkled with Zatar from Israel (mentioned in the old testament) and some cilantro and a touch of sweet pepper, and happened to be reading Archives of Internal Medicine published only yesterday and in it there were three studies in three different social contexts about the worth of diabetes education and cognitive changes that help those struggling over the years to control their diabetes. Lo and behold, the education was much better than many of the newer medications for Diabetes! Hats off to our cadre of Diabetes Educators. I rushed with the news to my colleagues who were doing just that over their lunchtime, educating a group of Indian patients with Diabetes… I shared the news with them.
The Indians had a big smile on their faces!
Friday, 30 September 2011
SEPTEMBER HAS BEEN A GOOD MONTH TO TRAVEL , FRIENDS AND DINNERS
Sept 1 left Miami for Bangalore via Frankfurt.
Sept 5 Bangalore to Kuala Lumpur
Sept 9/10 Malacca
Sept 11 Kuala Lumpur to Singapour
Sept 11 Singapour to London
Sept 12 London to Paris
Sept 18 Paris to London
Sept 19 London to Miami
Sept 21 Miami to Oklahoma City
Sept 22 Oklahoma City to Omaha
Sept 23-29 With American Indians
Sept 30 Back to Miami
The conversations which were memorable : Dr Li KL, Dr Tan and Mrs Irene G in Malacca, Family in Paris, Family in Miami, Steve Avery in Sioux City, Hocank and UmonHon Indians in the Indian country
Good Food to remember: Coconut Grove in Bangalore; Ole Sayang Nyonya in Malacca, Maroosh in Miami, Vivace in Omaha and LAN in Miami
Grateful for every one who made this month special. Merci Beaucoup!
Wednesday, 14 September 2011
RICE AND DIABETES
White Rice, Brown Rice, and Risk of Type 2 Diabetes in US Men and Women
Qi Sun, MD, ScD; Donna Spiegelman, ScD; Rob M. van Dam, PhD; Michelle D. Holmes, MD, DrPH; Vasanti S. Malik, MSc; Walter C. Willett, MD, DrPH; Frank B. Hu, MD, PhD
Arch Intern Med. 2010;170(11):961-969.
Background Because of differences in processing and nutrients, brown rice and white rice may have different effects on risk of type 2 diabetes mellitus. We examined white and brown rice consumption in relation to type 2 diabetes risk prospectively in the Health Professionals Follow-up Study and the Nurses' Health Study I and II.
Methods We prospectively ascertained and updated diet, lifestyle practices, and disease status among 39 765 men and 157 463 women in these cohorts.
Results After multivariate adjustment for age and other lifestyle and dietary risk factors, higher intake of white rice (5 servings per week vs <1 per month) was associated with a higher risk of type 2 diabetes: pooled relative risk (95% confidence interval [CI]), 1.17 (1.02-1.36). In contrast, high brown rice intake (2 servings per week vs <1 per month) was associated with a lower risk of type 2 diabetes: pooled relative risk, 0.89 (95% CI, 0.81-0.97). We estimated that replacing 50 g/d (uncooked, equivalent to one-third serving per day) intake of white rice with the same amount of brown rice was associated with a 16% (95% CI, 9%-21%) lower risk of type 2 diabetes, whereas the same replacement with whole grains as a group was associated with a 36% (30%-42%) lower diabetes risk.
Conclusions Substitution of whole grains, including brown rice, for white rice may lower risk of type 2 diabetes. These data support the recommendation that most carbohydrate intake should come from whole grains rather than refined grains to help prevent type 2 diabetes.
Qi Sun, MD, ScD; Donna Spiegelman, ScD; Rob M. van Dam, PhD; Michelle D. Holmes, MD, DrPH; Vasanti S. Malik, MSc; Walter C. Willett, MD, DrPH; Frank B. Hu, MD, PhD
Arch Intern Med. 2010;170(11):961-969.
Background Because of differences in processing and nutrients, brown rice and white rice may have different effects on risk of type 2 diabetes mellitus. We examined white and brown rice consumption in relation to type 2 diabetes risk prospectively in the Health Professionals Follow-up Study and the Nurses' Health Study I and II.
Methods We prospectively ascertained and updated diet, lifestyle practices, and disease status among 39 765 men and 157 463 women in these cohorts.
Results After multivariate adjustment for age and other lifestyle and dietary risk factors, higher intake of white rice (5 servings per week vs <1 per month) was associated with a higher risk of type 2 diabetes: pooled relative risk (95% confidence interval [CI]), 1.17 (1.02-1.36). In contrast, high brown rice intake (2 servings per week vs <1 per month) was associated with a lower risk of type 2 diabetes: pooled relative risk, 0.89 (95% CI, 0.81-0.97). We estimated that replacing 50 g/d (uncooked, equivalent to one-third serving per day) intake of white rice with the same amount of brown rice was associated with a 16% (95% CI, 9%-21%) lower risk of type 2 diabetes, whereas the same replacement with whole grains as a group was associated with a 36% (30%-42%) lower diabetes risk.
Conclusions Substitution of whole grains, including brown rice, for white rice may lower risk of type 2 diabetes. These data support the recommendation that most carbohydrate intake should come from whole grains rather than refined grains to help prevent type 2 diabetes.
METFORMIN EFFECT ON TSH HYPOTHYROIDISM
Thyroidal Effect of Metformin Treatment in Patients With Polycystic Ovary Syndrome
Mario Rotondi; Carlo Cappelli; Flavia Magri; Roberta Botta; Rosa Dionisio; Carmelo Iacobello; Pasquale De Cata; Rossella E. Nappi; Maurizio Castellano; Luca Chiovato
Authors and Disclosures
Posted: 09/09/2011; Clin Endocrinol. 2011;75(3):378–381 © 2011 Blackwell Publishing
Metformin is widely used for the treatment of type 2 diabetes. Growing evidence supports the beneficial effects of metformin also in patients with polycystic ovary syndrome (PCOS). It was recently reported that metformin has a TSH-lowering effect in hypothyroid patients with diabetes being treated with metformin.
Aim of this study was to evaluate the effect of metformin treatment on the thyroid hormone profile in patients with PCOS.
Patients and measurements Thirty-three patients with PCOS were specifically selected for being either treated with levothyroxine for a previous diagnosis of hypothyroidism (n = 7), untreated subclinically hypothyroid (n = 2) or euthyroid without levothyroxine treatment (n = 24) before the starting of metformin. The serum levels of TSH and FT4 were measured before and after a 4-month period of metformin therapy.
Results Thyroid function parameters did not change after starting metformin therapy in euthyroid patients with PCOS. In the 9 hypothyroid patients with PCOS, the basal median serum levels of TSH (3·2 mIU/l, range = 0·4–7·1 mIU/l) significantly (P < 0·05) decreased after a 4-month course of metformin treatment (1·7 mIU/l, range = 0·5–5·2 mIU/l). No significant change in the serum levels of FT4 was observed in these patients. The TSH-lowering effect of metformin was not related to the administered dose of the drug, which was similar in euthyroid as compared with hypothyroid patients with PCOS (1406 ± 589 vs 1322 ± 402 mg/day, respectively; NS).
Conclusions These results indicate that metformin treatment has a TSH-lowering effect in hypothyroid patients with PCOS, both treated with l-thyroxine and untreated.
Introduction
Metformin is a widely used drug for the treatment of type 2 diabetes. Metformin is commonly regarded as safe drug, because no clinically relevant pharmacologic interaction was described with most of the commonly used drugs, with the exception of folate and vitamin B12.[1–3] With specific regard to polycystic ovary syndrome (PCOS), metformin is not licensed for the treatment of this condition in any country to date.[4] Nevertheless, in the last few years, growing evidence supported beneficial effects of metformin in PCOS.[5,6] These studies prompted consensus statements and recommendations for the use of metformin in patients with PCOS.[7–10]
Despite the fact that metformin was introduced nearly 50 years ago in the clinical practice for the treatment of diabetes, only recently has this drug was reported to modify the thyroid hormone profile,[11–13] producing a significant decrease in the serum levels of TSH. Vigersky et al. [11] described four patients with primary hypothyroidism, being euthyroid on l-thyroxine (LT4), in whom the administration of metformin led to a significant fall in the serum levels of TSH. In these patients, the serum levels of FT4 were unchanged, and no clinical sign of thyrotoxicosis was observed. The effect of metformin was found to be reversible, because drug withdrawal was accompanied by a significant rise in serum TSH levels, which returned to the premetformin serum concentration.[11] More recently, it was demonstrated that the TSH-lowering effect of metformin is also observed in primary hypothyroid patients with diabetes and primary hypothyroidism, who are not treated with L-T4 replacement therapy.[13]
Despite the clinical relevance of these findings, the mechanisms by which metformin produces a TSH-lowering effect remain largely unknown. To further characterise the effect of metformin treatment on circulating thyroid function parameters, we investigated the impact of metformin treatment on the serum levels of thyroid hormones and TSH in a cohort of patients with PCOS, both euthyroid or hypothyroid
Mario Rotondi; Carlo Cappelli; Flavia Magri; Roberta Botta; Rosa Dionisio; Carmelo Iacobello; Pasquale De Cata; Rossella E. Nappi; Maurizio Castellano; Luca Chiovato
Authors and Disclosures
Posted: 09/09/2011; Clin Endocrinol. 2011;75(3):378–381 © 2011 Blackwell Publishing
Metformin is widely used for the treatment of type 2 diabetes. Growing evidence supports the beneficial effects of metformin also in patients with polycystic ovary syndrome (PCOS). It was recently reported that metformin has a TSH-lowering effect in hypothyroid patients with diabetes being treated with metformin.
Aim of this study was to evaluate the effect of metformin treatment on the thyroid hormone profile in patients with PCOS.
Patients and measurements Thirty-three patients with PCOS were specifically selected for being either treated with levothyroxine for a previous diagnosis of hypothyroidism (n = 7), untreated subclinically hypothyroid (n = 2) or euthyroid without levothyroxine treatment (n = 24) before the starting of metformin. The serum levels of TSH and FT4 were measured before and after a 4-month period of metformin therapy.
Results Thyroid function parameters did not change after starting metformin therapy in euthyroid patients with PCOS. In the 9 hypothyroid patients with PCOS, the basal median serum levels of TSH (3·2 mIU/l, range = 0·4–7·1 mIU/l) significantly (P < 0·05) decreased after a 4-month course of metformin treatment (1·7 mIU/l, range = 0·5–5·2 mIU/l). No significant change in the serum levels of FT4 was observed in these patients. The TSH-lowering effect of metformin was not related to the administered dose of the drug, which was similar in euthyroid as compared with hypothyroid patients with PCOS (1406 ± 589 vs 1322 ± 402 mg/day, respectively; NS).
Conclusions These results indicate that metformin treatment has a TSH-lowering effect in hypothyroid patients with PCOS, both treated with l-thyroxine and untreated.
Introduction
Metformin is a widely used drug for the treatment of type 2 diabetes. Metformin is commonly regarded as safe drug, because no clinically relevant pharmacologic interaction was described with most of the commonly used drugs, with the exception of folate and vitamin B12.[1–3] With specific regard to polycystic ovary syndrome (PCOS), metformin is not licensed for the treatment of this condition in any country to date.[4] Nevertheless, in the last few years, growing evidence supported beneficial effects of metformin in PCOS.[5,6] These studies prompted consensus statements and recommendations for the use of metformin in patients with PCOS.[7–10]
Despite the fact that metformin was introduced nearly 50 years ago in the clinical practice for the treatment of diabetes, only recently has this drug was reported to modify the thyroid hormone profile,[11–13] producing a significant decrease in the serum levels of TSH. Vigersky et al. [11] described four patients with primary hypothyroidism, being euthyroid on l-thyroxine (LT4), in whom the administration of metformin led to a significant fall in the serum levels of TSH. In these patients, the serum levels of FT4 were unchanged, and no clinical sign of thyrotoxicosis was observed. The effect of metformin was found to be reversible, because drug withdrawal was accompanied by a significant rise in serum TSH levels, which returned to the premetformin serum concentration.[11] More recently, it was demonstrated that the TSH-lowering effect of metformin is also observed in primary hypothyroid patients with diabetes and primary hypothyroidism, who are not treated with L-T4 replacement therapy.[13]
Despite the clinical relevance of these findings, the mechanisms by which metformin produces a TSH-lowering effect remain largely unknown. To further characterise the effect of metformin treatment on circulating thyroid function parameters, we investigated the impact of metformin treatment on the serum levels of thyroid hormones and TSH in a cohort of patients with PCOS, both euthyroid or hypothyroid
SHORT TERM INTENSIVE THERAPY FOR NEWLY DIAGNOSED TYPE 2 DIABETES
Short-term Intensive Therapy in Newly Diagnosed Type 2 Diabetes Partially Restores Both Insulin Sensitivity and Beta-Cell Function in Subjects With Long-term Remission
Hu Y, Li L, Xu Y, et al.
Diabetes Care. 2011;34:1848-1853
Study Summary
The goal of this Chinese study was to examine the effect of intensive glycemic control therapy (IT) on insulin sensitivity and beta-cell function in newly diagnosed type 2 diabetic patients compared with persons with normal glucose tolerance (NGT) and those with impaired glucose tolerance (IGT). Investigators assigned 48 newly diagnosed type 2 diabetic patients to IT (continuous subcutaneous insulin infusion, multiple daily injections, or oral hypoglycemic agents) with the goal of achieving fasting plasma glucose (FPG) < 6.1 mmol/L (110 mg/dL) and postprandial glucose (PPG) < 8.0 mmol/L (144 mg/dL). Treatments were maintained for 2 weeks after the target was achieved, and patients were followed for 1 year. Hyperglycemia relapse was defined as FPG > 7.0 mmol/L (126 mg/dL) or PPG > 11.0 mmol/L (198 mg/dL). Patients who maintained optimal glycemic control for at least 12 months without medication were defined as being in remission, and those who relapsed during the 1-year follow-up were defined as nonremission. Those in remission received no medication, whereas the relapsed patients resumed oral hyperglycemic agents or IT during the 1-year follow-up period. Homeostasis model assessment (HOMA) was used to estimate insulin resistance (HOMA-IR), beta cell function (HOMA-beta) and the disposition index.
After short-term IT, 21 of 48 newly diagnosed type 2 diabetic patients (44%) achieved remission for 1 year, and 27 patients had relapsed (nonremission). There were no apparent differences in therapeutic effectiveness among the 3 different therapies. Before IT, HOMA-IR in both remission (3.12 ± 1.4 [mean +/= SD]) and nonremission (2.70 ± 1.7) groups was significantly higher than that in IGT (1.96 ± 1.1) and NGT (1.37 ± 0.6) persons. After IT, HOMA-IR in the remission group after treatment (1.72 ± 0.8) and at 1 year (2.12 ± 1.3) was comparable with that in IGT and NGT groups (P > .05). However, in the nonremission group, HOMA-IR was reduced from 2.70 ± 1.7 before IT to 2.34 ± 1.4 immediately after IT and to 2.60 ± 1.9 at the 1-year follow-up. IT restored more HOMA-beta in the remission group (44.6 [95% CI, 32.1-69.1] after therapy; 51.9 [28.8-79.8] at 1 year) than in the nonremission group (26.5 [14.9-43.8] after therapy; 31.9 [18.8-52.7] at 1 year). Although more restoration of HOMA-beta was observed in the remission group than in the nonremission group, there was no statistical difference. Disposition index in the remission group was significantly higher than that in the nonremission group after IT and at 1 year.
Viewpoint
Glycemic control is fundamental to the management of diabetes with the objective of (safely) reducing hyperglycemia to as near normal as possible.[1] The current recommendation for newly diagnosed patients is immediate initiation of metformin.[2] However, studies have shown that early intensive insulin therapy can induce and maintain diabetes remission.[3,4] One important and interesting finding of the current study is that similar remission was achieved with oral agents (metformin plus gliclazide if necessary) as with insulin. Treating diabetes intensively at diagnosis, regardless of therapy, achieved a 1-year remission rate of 44%. Thus, for the patient who wants to try lifestyle modification without drugs, as many do, it appears that such a strategy might be effective after first aggressively reducing hyperglycemia. Another interesting finding was that for patients who achieved remission, insulin sensitivity was nearly fully restored, but beta-cell function was only modestly improved after intensive therapy. This may therefore be an important marker of who can maintain glucose control with lifestyle-only therapy following a course of intensive glucose reduction.
Hu Y, Li L, Xu Y, et al.
Diabetes Care. 2011;34:1848-1853
Study Summary
The goal of this Chinese study was to examine the effect of intensive glycemic control therapy (IT) on insulin sensitivity and beta-cell function in newly diagnosed type 2 diabetic patients compared with persons with normal glucose tolerance (NGT) and those with impaired glucose tolerance (IGT). Investigators assigned 48 newly diagnosed type 2 diabetic patients to IT (continuous subcutaneous insulin infusion, multiple daily injections, or oral hypoglycemic agents) with the goal of achieving fasting plasma glucose (FPG) < 6.1 mmol/L (110 mg/dL) and postprandial glucose (PPG) < 8.0 mmol/L (144 mg/dL). Treatments were maintained for 2 weeks after the target was achieved, and patients were followed for 1 year. Hyperglycemia relapse was defined as FPG > 7.0 mmol/L (126 mg/dL) or PPG > 11.0 mmol/L (198 mg/dL). Patients who maintained optimal glycemic control for at least 12 months without medication were defined as being in remission, and those who relapsed during the 1-year follow-up were defined as nonremission. Those in remission received no medication, whereas the relapsed patients resumed oral hyperglycemic agents or IT during the 1-year follow-up period. Homeostasis model assessment (HOMA) was used to estimate insulin resistance (HOMA-IR), beta cell function (HOMA-beta) and the disposition index.
After short-term IT, 21 of 48 newly diagnosed type 2 diabetic patients (44%) achieved remission for 1 year, and 27 patients had relapsed (nonremission). There were no apparent differences in therapeutic effectiveness among the 3 different therapies. Before IT, HOMA-IR in both remission (3.12 ± 1.4 [mean +/= SD]) and nonremission (2.70 ± 1.7) groups was significantly higher than that in IGT (1.96 ± 1.1) and NGT (1.37 ± 0.6) persons. After IT, HOMA-IR in the remission group after treatment (1.72 ± 0.8) and at 1 year (2.12 ± 1.3) was comparable with that in IGT and NGT groups (P > .05). However, in the nonremission group, HOMA-IR was reduced from 2.70 ± 1.7 before IT to 2.34 ± 1.4 immediately after IT and to 2.60 ± 1.9 at the 1-year follow-up. IT restored more HOMA-beta in the remission group (44.6 [95% CI, 32.1-69.1] after therapy; 51.9 [28.8-79.8] at 1 year) than in the nonremission group (26.5 [14.9-43.8] after therapy; 31.9 [18.8-52.7] at 1 year). Although more restoration of HOMA-beta was observed in the remission group than in the nonremission group, there was no statistical difference. Disposition index in the remission group was significantly higher than that in the nonremission group after IT and at 1 year.
Viewpoint
Glycemic control is fundamental to the management of diabetes with the objective of (safely) reducing hyperglycemia to as near normal as possible.[1] The current recommendation for newly diagnosed patients is immediate initiation of metformin.[2] However, studies have shown that early intensive insulin therapy can induce and maintain diabetes remission.[3,4] One important and interesting finding of the current study is that similar remission was achieved with oral agents (metformin plus gliclazide if necessary) as with insulin. Treating diabetes intensively at diagnosis, regardless of therapy, achieved a 1-year remission rate of 44%. Thus, for the patient who wants to try lifestyle modification without drugs, as many do, it appears that such a strategy might be effective after first aggressively reducing hyperglycemia. Another interesting finding was that for patients who achieved remission, insulin sensitivity was nearly fully restored, but beta-cell function was only modestly improved after intensive therapy. This may therefore be an important marker of who can maintain glucose control with lifestyle-only therapy following a course of intensive glucose reduction.
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