Stearoyl-CoA desaturase-1 is associated with insulin resistance in morbidly obese subjects.

Animal studies have revealed the association between stearoyl-CoA desaturase 1 (SCD1) and obesity and insulin resistance. However, only a few studies have been undertaken in humans. We studied SCD1 in visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) from morbidly obese patients and their association with insulin resistance, sterol regulatory element binding protein-1 (SREBP-1) and ATPase p97, proteins involved in SCD1 synthesis and degradation. The insulin resistance was calculated in 40 morbidly obese patients and 11 overweight controls. Measurements were made of VAT and SAT SCD1, SREBP-1 and ATPase p97 mRNA expression and protein levels. VAT and SAT SCD1 mRNA expression levels in the morbidly obese patients were significantly lower than in the controls (P = 0.006), whereas SCD1 protein levels were significantly higher (P < 0.001). In the morbidly obese patients, the VAT SCD1 protein levels were decreased in patients with higher insulin resistance (P = 0.007). However, SAT SCD1 protein levels were increased in morbidly obese patients with higher insulin resistance (P < 0.05). Multiple linear regressions in the morbidly obese patients showed that the variable associated with the SCD1 protein levels in VAT was insulin resistance, and the variables associated with SCD1 protein levels in SAT were body mass index (BMI) and ATPase p97. In conclusion, these data suggest that the regulation of SCD1 is altered in individuals with morbid obesity and that the SCD1 protein has a different regulation in the two adipose tissues, as well as being closely linked to the degree of insulin resistance.

Changes in the serum composition of free-fatty acids during an intravenous glucose tolerance test.

Recent studies suggest that measuring the free-fatty acids (FFA) during an intravenous glucose tolerance test (IVGTT) may provide information about the metabolic associations between serum FFA and carbohydrate and insulin metabolism. We evaluated the FFA profile during an IVGTT and determined whether this test changes the composition and concentration of FFA. An IVGTT was given to 38 severely obese persons before and 7 months after undergoing bariatric surgery and also to 12 healthy, nonobese persons. The concentration and composition of the FFA were studied at different times during the test. The concentration of FFA fell significantly faster during the IVGTT in the controls and in the severely obese persons with normal-fasting glucose (NFG) than in the severely obese persons with impaired-fasting glucose (IFG) or type 2 diabetes mellitus (T2DM) (P < 0.05). Significant differences were found in the time to minimum serum concentrations of FFA (control = NFG < IFG < T2DM) (P < 0.001). These variables improved after bariatric surgery in the three groups. The percentage of monounsaturated and n-6 polyunsaturated FFA in the control subjects and in the obese persons, both before and after surgery, decreased significantly during the IVGTT. In conclusion, during an IVGTT, severely obese persons with IFG or T2DM experienced a lower fall in the FFA than the severely obese persons with NFG and the controls, becoming normal after bariatric surgery.

Plasma visfatin concentrations in severely obese subjects are increased after intestinal bypass.

OBJECTIVE: Visfatin has shown to be increased in obesity and in type 2 diabetes. The aim of this study was to determine the change in plasma visfatin in severely obese (SO) persons after weight loss following bariatric surgery in relation to glucose concentration. RESEARCH METHODS AND PROCEDURES: Visfatin and leptin were studied in 53 SO persons (BMI, 54.4 +/- 6.8 kg/m(2)) before and 7 months after bariatric surgery and in 28 healthy persons (BMI, 26.8 +/- 3.8 kg/m(2)). All of the patients underwent bariatric surgery with biliopancreatic diversion or gastric bypass. RESULTS: The pre-surgery levels of visfatin in the SO group were greater than in the control group (55.9 +/- 39.9 vs. 42.9 +/- 16.6 ng/mL, p = 0.024). This increase was significant in the SO group with impaired fasting glucose (63.4 +/- 36.6 ng/mL) and diabetes (60.0 +/- 46.0 ng/mL). SO patients with normal fasting glucose had similar levels of visfatin to the controls. Seven months after surgery, visfatin levels were significantly increased (84.8 +/- 32.8 ng/mL, p < 0.001). This increase was independent of the pre-surgical glucose levels. The type of bariatric surgery had no influence on visfatin levels. Post-surgical visfatin was significantly correlated with the post-surgery plasma concentrations of leptin (r = 0.39, p = 0.014). DISCUSSION: Plasma levels of visfatin in the SO group were increased but only when accompanied by high glucose levels, even in the range of impaired fasting glucose. Bariatric surgery causes an increase in visfatin, which is correlated mainly with the changes produced in the leptin concentration.

Morbidly obese individuals with impaired fasting glucose have a specific pattern of insulin secretion and sensitivity: effect of weight loss after bariatric surgery.

BACKGROUND: Obesity is often associated with hyper-secrection of insulin. Impaired fasting glucose (IFG) has recently been redefined as a fasting plasma glucose of 5.6-6.9 mmol/L. The aim of this study was to determine whether changes in insulin secretion in morbidly obese persons also commence with normal serum glucose levels. METHODS: 32 morbidly obese subjects were studied before and after bariatric surgery. Measurements were made of glucose tolerance (K(G)), insulin sensitivity (SI), first-phase insulin release and the disposition index (DI) from a frequently sampled intravenous glucose tolerance test. RESULT: In morbidly obese subjects, the SI (P<0.01), DI (P<0.01) and first-phase insulin release (P<0.02) started changing with serum glucose levels considered to be normal (5.00-5.28 mmol/L). K(G) showed a clear slope according to the baseline glycemia status (P<0.05), and it was significantly related with the DI, both before (r=0.76, P<0.001) and after (r=0.57, P=0.002) surgery. Following surgery, all the variables significantly associated with insulin secretion and insulin sensitivity recovered significantly. The most significant changes occurred in morbidly obese individuals with IFG. CONCLUSIONS: Morbidly obese subjects show slopes of insulin sensitivity and insulin secretion in accordance with their baseline serum glucose levels. The fall in first-phase insulin release begins when serum glucose values are considered normal. Morbidly obese persons with the IFG phenotype have a specific pattern of insulin sensitivity and insulin secretion. K(G) clearly discriminates the clinical phenotypes, depending on baseline serum glucose levels.