title: Visceral fat in hypertension: influence on insulin resistance and beta-cell function.
abstract: Preferential visceral adipose tissue (VAT) deposition has been associated with the presence of insulin resistance in obese and diabetic subjects. The independent association of VAT accumulation with hypertension and its impact on insulin sensitivity and beta-cell function have not been assessed. We measured VAT and subcutaneous fat depots by multiscan MRI in 13 nondiabetic men with newly detected, untreated essential hypertension (blood pressure=151+/-2/94+/-2 mm Hg, age=47+/-2 years, body mass index [BMI]=28.4+/-0.7 kg x m(-2)) and 26 age-matched and BMI-matched normotensive men (blood pressure=123+/-1/69+/-2 mm Hg). Insulin secretion was measured by deconvolution of C-peptide data obtained during an oral glucose tolerance test, and dynamic indices of beta-cell function were calculated by mathematical modeling. For a similar fat mass in the scanned abdominal region (4.8+/-0.3 versus 3.9+/-0.3 kg, hypertensive subjects versus controls, P=0.06), hypertensive subjects had 60% more VAT than controls (1.6+/-0.2 versus 1.0+/-0.1 kg, P=0.003). Intrathoracic fat also was expanded in patients versus controls (45+/-5 versus 28+/-3 cm2, P=0.005). Insulin sensitivity was reduced (10.7+/-0.7 versus 12.9+/-0.4 mL x min(-1) x kg(ffm)(-1), P=0.006), and total insulin output was proportionally increased (64 [21] versus 45 [24] nmol x m(-2). h, median [interquartile range], P=0.01), but dynamic indices of beta-cell function (glucose sensitivity, rate sensitivity, and potentiation) were similar in the 2 groups. Abdominal VAT, insulin resistance, and blood pressure were quantitatively interrelated (rho's of 0.39 to 0.47, P<0.02 or less). In newly found, untreated men with essential hypertension, fat is preferentially accumulated intraabdominally and intrathoracically. Such visceral adiposity is quantitatively related to both height of blood pressure and severity of insulin resistance, but has no impact on the dynamics of beta-cell function.
authors.affiliation: National Research Council, Institute of Clinical Physiology, Area of research, Via Moruzzi, 1 S. Cataldo, 56100 Pisa, Italy. sironi@ifc.cnr.it
authors.forename: Anna Maria
authors.initials: AM
authors.lastname: Sironi
authors.forename: Amalia
authors.initials: A
authors.lastname: Gastaldelli
authors.forename: Andrea
authors.initials: A
authors.lastname: Mari
authors.forename: Demetrio
authors.initials: D
authors.lastname: Ciociaro
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Positano
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Postano
authors.forename: Emma
authors.initials: E
authors.lastname: Buzzigoli
authors.forename: Sergio
authors.initials: S
authors.lastname: Ghione
authors.forename: Stefano
authors.initials: S
authors.lastname: Turchi
authors.forename: Massimo
authors.initials: M
authors.lastname: Lombardi
authors.forename: Ele
authors.initials: E
authors.lastname: Ferrannini
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D000368:Aged; D000886:Anthropometry; D019540:Area Under Curve; D005947:Glucose / Q000493:pharmacokinetics; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D008297:Male; D008482:Mediastinum; D008875:Middle Aged; D009765:Obesity / Q000150:complications / Q000378:metabolism
chemical_list: D007328:Insulin; D005947:Glucose