Improvement of insulin resistance and early atherosclerosis in patients after gastric banding.
OBJECTIVE
To evaluate the effect of massive weight loss on insulin sensitivity, soluble adhesion molecules, and markers of the insulin resistance syndrome (IRS).


METHODS
Eighteen morbidly obese patients underwent gastric banding and were evaluated before and 6 and 12 months after surgery. Total insulin secretion, hepatic insulin extraction, and insulin sensitivity were analyzed by oral glucose-tolerance test model analysis. In addition, soluble intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, leptin, high-sensitivity C-reactive protein, plasminogen activating factor-1 (PAI-1), and tissue plasminogen activator were measured.


RESULTS
BMI dropped from 45.22 +/- 5.62 to 36.99 +/- 4.34 kg/m(2) after 6 months and 33.72 +/- 5.55 kg/m(2) after 12 months (both p < 0.0001). This intervention resulted in a significant reduction of blood pressure (p < 0.00001), triglycerides (p < 0.01), fasting blood glucose (p = 0.03), basal insulin (p < 0.001), and basal C-peptide (p = 0.008) levels. Total insulin secretion decreased (p < 0.05), whereas hepatic insulin extraction (p < 0.05) and oral glucose insulin sensitivity index (p < 0.0001) increased compared with baseline. Leptin (p < 0.0001) and E-selectin levels decreased significantly after 6 and 12 months (p = 0.05), whereas significantly lower levels of intercellular adhesion molecule-1 and PAI-1 were only seen after 6 months. Subclinical inflammation, measured by high-sensitivity C-reactive protein, was lowered to normal ranges. No changes were observed in vascular cell adhesion molecule-1 and tissue plasminogen activator levels.


CONCLUSIONS
Although gastric banding ameliorates several features of the IRS, including 29.05% improvement in insulin sensitivity and blood pressure and reduction of soluble adhesion molecules and PAI-1, considerable weight loss did not normalize all components of the IRS in morbidly obese patients.
Department of Internal Medicine V, Division of Endocrinology and Metabolism, Wilhelminenspital, Vienna, Austria. c.enserer@utanet.at
Ursula
U
Hanusch-Enserer
Edmund
E
Cauza
Marita
M
Spak
Georg
G
Endler
Attila
A
Dunky
Andrea
A
Tura
Oswald
O
Wagner
Harald R
HR
Rosen
Giovanni
G
Pacini
Rudolf
R
Prager
D000328:Adult; D001161:Arteriosclerosis / Q000097:blood* / Q000534:rehabilitation; D002096:C-Peptide / Q000097:blood; D015815:Cell Adhesion Molecules / Q000097:blood; D019040:E-Selectin / Q000097:blood; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D006973:Hypertension / Q000628:therapy; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance / Q000502:physiology*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D009767:Obesity, Morbid / Q000097:blood* / Q000534:rehabilitation / Q000601:surgery; D010960:Plasminogen Activators / Q000097:blood; D013270:Stomach / Q000601:surgery; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D015431:Weight Loss / Q000502:physiology*
D002096:C-Peptide; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D007328:Insulin; D020738:Leptin; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D010960:Plasminogen Activators