General Practitioners, Internist, Endocrinologist (diabetes, hormones)
25 years of experience

Accepting new patients
Multispecialty Center & Stark Diabetes Clinic
2660 Gulf Fwy S
Victory Lakes, League City, TX 77573
832-505-2000
Locations and availability (5)

Education ?

Medical School
Univ Di Modena, Fac Di Med E Chirurgia, Modena, Italy (1985)

Affiliations ?

Dr. Abate is affiliated with 7 hospitals.

Hospital Affilations

Score

Rankings

  • University of Texas Medical Branch
    301 University Blvd, Galveston, TX 77555
    • Currently 4 of 4 crosses
    Top 25%
  • UT Southwestern University Hospital - Zale Lipshy
    5151 Harry Hines Blvd, Dallas, TX 75235
    • Currently 4 of 4 crosses
    Top 25%
  • Parkland Health & Hospital System
    5201 Harry Hines Blvd, Dallas, TX 75235
    • Currently 1 of 4 crosses
  • Dallas County Hospital District
  • Utmb, Galveston
  • Parkland Health and Hospital System
  • UT Southwestern Zale Lipshy Hospital
  • Publications & Research

    Dr. Abate has contributed to 2 publications.
    Title Effect of Angiotensin Receptor Blockade on Insulin Sensitivity and Endothelial Function in Abdominally Obese Hypertensive Patients with Impaired Fasting Glucose.
    Date December 2011
    Journal Clinical Science (london, England : 1979)
    Excerpt

    AngII (angiotensin II) may contribute to cardiovascular risk in obesity via adverse effects on insulin sensitivity and endothelial function. In the present study, we examined the effects of ARB (angiotensin receptor blocker) therapy (losartan, 100 mg/day) on insulin sensitivity and endothelial function in 53 subjects with stage I hypertension, abdominal obesity and impaired fasting glucose. The study design was a randomized double-blinded parallel design placebo-controlled multi-centre trial of 8 weeks duration. We used the hyperinsulinaemic-euglycaemic clamp technique to measure insulin sensitivity (expressed as the 'M/I' value) and RH-PAT (reactive hyperaemia-peripheral arterial tonometry) to measure endothelial function. Additional measures included HOMA (homoeostasis model assessment)-B, an index of pancreatic β-cell function, and markers of inflammation [e.g. CRP (C-reactive protein)] and oxidative stress (e.g. F2-isoprostanes). ARB therapy did not alter insulin sensitivity [5.2 (2.7) pre-treatment and 4.6 (1.6) post-treatment] compared with placebo therapy [6.1 (2.9) pre-treatment and 5.3 (2.7) post-treatment; P value not significant], but did improve the HOMA-B compared with placebo therapy (P=0.05). ARB therapy also did not change endothelial function [RH-PAT, 2.15 (0.7) pre-treatment and 2.11 (0.7) post-treatment] compared with placebo therapy [RH-PAT, 1.81 (0.5) pre-treatment and 1.76 (0.7) post-treatment; P value not significant]. Markers of inflammation and oxidative stress were not significantly changed by ARB therapy. In conclusion, ARB therapy did not alter peripheral insulin sensitivity or endothelial function in this cohort of patients with essential hypertension, abdominal obesity and impaired fasting glucose, but did improve pancreatic β-cell function.

    Title Overweight and Sympathetic Overactivity in Black Americans.
    Date October 2001
    Journal Hypertension
    Excerpt

    A large body of clinical investigation implicates an important role for the sympathetic nervous system in linking obesity with hypertension. However, the experimental support for this hypothesis is derived from strictly white cohorts. The goal of this study was to determine whether being overweight begets sympathetic overactivity in black Americans, the ethnic minority at highest risk for hypertension. We recorded postganglionic sympathetic nerve discharge with microelectrodes in muscle nerve fascicles of the peroneal nerve in 92 normotensive young adult black men and women within a wide range of body mass index. The same experiments were performed in a control group of 45 normotensive white men and women of similar ages and body mass indices. The major new findings are 2-fold. First, in young, normotensive, overtly healthy black women, being overweight begets sympathetic overactivity (r=0.45, P=0.0009), a putative intermediate phenotype for incident hypertension. Second, in black men, sympathetic nerve discharge is dissociated from body mass index (r=0.03, P=NS). This dissociation is explained in part by a 20% to 40% higher rate of sympathetic nerve discharge in lean black men compared with lean white men and lean black and white women (28+/-3 versus 18+/-2, 21+/-2, and 17+/-2 bursts/min, respectively; P<0.05). Sympathetic nerve discharge in lean black men is comparable to that of overweight black men and women as well as white men and women. These data provide the first microneurographic evidence for tonic central sympathetic overactivity in blacks, both adiposity-related sympathetic overactivity in black women and adiposity-independent sympathetic overactivity in black men.

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