Judith Korner, MD, PhD, of Columbia University in New York City, and colleagues reported that, insulin secretion fell from 13.8 mcIU/mL to 6.8 mcIU/mL (P<0.001) in the diet group, compared with a drop from 23.1 mcIU/mL to 12.7 mcIU/mL (P<0.01) in the bariatric surgery group.
C-peptide, a measure of beta-cell function, dropped from 3.59 ng/mL to 2.55 ng/mL (P<0.01) in the diet group and from 3.72 ng/mL to 2.95 ng/mL (P<0.05) in the surgery group, they noted.
"Contrary to our expectations, this study demonstrates that Roux-en-Y gastric bypass [RYGB] in subjects with type 2 diabetes does not result in greater improvement in beta-cell function compared with equivalent weight loss achieved over the same period by a very-low-calorie diet," the authors wrote. "These data indicate that the changes in glucose homeostasis that occur within 2 to 3 weeks after RYGB are primarily due to very low energy intake, as opposed to specific surgically-induced hormonal effects."
But they cautioned that the results don’t suggest that gastric bypass is less beneficial in the long run, "since the degree of caloric restriction required to mimic surgical results cannot be maintained in most individuals."
Patients with type 2 diabetes who have gastric bypass surgery typically have marked improvement in glycemic control, even before they have major weight loss. For instance, glycemic control improves within the first 2 to 3 weeks after the procedure, before most weight loss occurs. This has led researchers to hypothesize that factors in addition to weight loss are involved in glycemic improvement.
To determine if the magnitude of this change is primarily due to caloric restriction or is unique to the surgical procedure, Korner and colleagues looked at 11 patients who had gastric bypass and compared them with 14 matched patients who were put on a very-low-calorie diet.
The patients in the diet group, who were evaluated as inpatients, ate a total of 500 calories per day with a macronutrient content similar to that of the diet given to patients after bypass surgery. At baseline, patients had a mean body mass index (BMI) of 41.2 kg/m2, their mean duration of diabetes was 5.7 years, and their mean glycated hemoglobin (HbA1c) was 8.4%.
The researchers performed intravenous glucose tolerance tests before and after the interventions.
Both groups lost an equivalent amount of weight over a mean study period of 21 days — 8.1% of body weight for gastric bypass patients and 7.2% for those on the very-low-calorie diet, which was not significantly different.
In addition to insulin secretion and C-peptide levels, Korner and colleagues found that other measures of insulin sensitivity and beta-cell function improved to a similar extent in both the bypass group and in the diet group, respectively:
- HOMA-IR: from 9.5 to 3.5 (P<0.01), and from 6.2 to 1.8 (P<0.001)
- Acute C-Peptide response: 12.1% to 28.5% (P<0.05), and from 12.1% to 24% (P<0.01)
- Declines in fasting glucose and fructosamine levels were similar between groups as well, they reported. In terms of gut hormones, there was a significant increase in adiponectin and in glucagon-like peptide-1 (GLP-1) for those in the gastric bypass group (P<0.05 for both), but not for those in the diet group.
- And with both approaches, as expected, plasma leptin levels decreased significantly for both the bypass group and the diet group (P<0.001 and P<0.01, respectively), they wrote.
Korner and colleagues concluded that a very-low-calorie diet improves insulin sensitivity and beta-cell function just as well as gastric bypass — at least in the short term.
- Be aware that this level of caloric restriction is unlikely to be feasible for most patients in the long term.
- Note that this cohort study demonstrated that similar weight, C-peptide, and insulin changes occurred in obese patients with diabetes undergoing gastric bypass and a matched group who received a 500-calorie-per-day diet.
Diabetes: Jackness C, et al "Very low calorie diet mimics the early beneficial effect of Roux-en-Y gastric bypass on insulin sensitivity and beta-cell function in type 2 diabetic patients" Diabetes 2013; DOI: 10.2337/db12-1762.