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Internist, Endocrinologist (diabetes, hormones), Geriatric Specialist (elderly care)
19 years of experience

Video profile


Education ?

Medical School
University of Tichreen (1993)

Awards & Distinctions ?

Top 10 Doctor - Metro Area (2014)
Phoenix Metro Area
Top 10 Doctor - State (2014)
On-Time Doctor Award (2015)
Hormone Foundation
American Association of Clinical Endocrinologists
American Board of Internal Medicine

Affiliations ?

Dr. Horani is affiliated with 8 hospitals.

Hospital Affiliations



  • St Joseph's Hospital
    350 W Thomas Rd, Phoenix, AZ 85013
    Top 25%
  • Arizona Heart Hospital
    1930 E Thomas Rd, Phoenix, AZ 85016
    Top 25%
  • CHANDLER REGIONAL Medical Center
    475 S Dobson Rd, Chandler, AZ 85224
    Top 25%
  • Banner Good Samaritan Regional Medical Center
    1111 E McDowell Rd, Phoenix, AZ 85006
    Top 25%
  • Mountain Vista Hospital
    1301 S Crismon Rd, Mesa, AZ 85209
  • Mercy Gilbert Medical Center
    3555 S Val Vista Dr, Gilbert, AZ 85297
  • St. Joseph`s Hospital and Medical Center - Phoenix
  • John C Lincoln Hospital NM
  • Publications & Research

    Dr. Horani has contributed to 15 publications.
    Title Secondary Cushing's Syndrome After a Single Epidural Injection of a Corticosteroid.
    Date November 2006
    Journal Endocrine Practice : Official Journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
    Title Saturated, Unsaturated, and Trans-fatty Acids Modulate Oxidative Burst Induced by High Dextrose in Human Umbilical Vein Endothelial Cells.
    Date July 2006
    Journal Nutrition (burbank, Los Angeles County, Calif.)

    OBJECTIVE: We determined whether hyperglycemia-induced oxidative burst is augmented in the presence of saturated, unsaturated, and trans-fatty acids (FAs). METHODS: The time course of superoxide (O2-) production in human umbilical vein endothelial cells treated with 5.5 mM (D100) or 27.5 mM (D500) of dextrose and select FAs were measured using the hydroethidene fluorescence method. RESULTS: The rate of O2- production in cells treated with D500 was significantly higher (55% to 125% increase) than the rate observed in control cells treated with D100 (P < 0.001). The rate of O2- production (mean +/- standard deviation, in arbitrary units) was increased when cells were treated with 250, 500, and 1000 muM of myristic acid (C14; 0.189 +/- 0.04, 0.240 +/- 0.04, 0.234 +/- 0.02, respectively; P > 0.1, P < 0.05, P < 0.05, respectively), palmitate (C16; 0.151 +/- 0.03, 0.218 +/- 0.01, 0.289 +/- 0.07; P > 0.1, P < 0.05, P < 0.01), and stearic acid (C18; 0.321 +/- 0.03, 0.259 +/- 0.02, 0.341 +/- 0.03; P < 0.01 for all comparisons) compared with control cells treated with D100 only (0.184 +/- 0.01). In the presence of D500, myristic acid did not significantly augment O2- production, whereas stearic acid caused a significant further increase in O2- production. The cis unsaturated FA (oleic, C18:1; linoleic, C18:2; or linolenic acid, C18:3) stimulated O2- production significantly more than did saturated FA or trans-unsaturated FA such as elaidic, linolelaidic, or linolenelaidic acid. CONCLUSIONS: Fatty acids have the ability to modulate oxidative load in hyperglycemia and this effect may be related to the length, saturation, and possibly cis/trans orientation of the FA.

    Title Suppression of Hyperglycemia-induced Superoxide Formation and Endothelin-1 Gene Expression by Carvedilol.
    Date May 2006
    Journal American Journal of Therapeutics

    Carvedilol (CV) is a beta-blocker with favorable effects on cardiovascular disease. To determine whether CV can prevent increases in superoxide (SO) production due to hyperglycemia, human umbilical vein endothelial cells (HUVEC) were treated with either 100 or 500 mg/dL dextrose in the presence or absence of 0.1, 1.0, and 10 micromol/L CV. Superoxide levels were measured using the hydroethidine (HE) fluorescence method. Generation of SO was linear from time 0 to 60 minutes. At 60 minutes, the HE fluorescence in cells treated with 500 mg/dL dextrose (123.3+/-4.9 units) was significantly higher than that in control cells treated with 100 mg/dL dextrose (84.0+/-3.5 units) (P<0.002). Addition of 0.1, 1.0, and 10 micromol/L CV to cells treated with 500 mg/dL dextrose decreased SO generated to 113.3+/-1.8, 98.7+/-8.3, and 70.0+/-1.0 units, respectively (P<0.13, P<0.05, and P<0.004, respectively). Cellular endothelin-1 mRNA and endothelin-1 protein secreted in culture media were significantly increased in the presence of 500 mg/dL dextrose. The addition of 10 micromol/L CV significantly decreased both endothelin-1 (1-21) mRNA and protein levels. Measurements of media lactate dehydrogenase activity indicated that CV inhibited cytotoxicity caused by 500 mg/dL dextrose. These findings suggest that CV not only prevents dextrose-induced SO generation in endothelial cells but may also have favorable effects on gene expression and cell survival.

    Title Statins Prevent Dextrose-induced Endothelial Barrier Dysfunction, Possibly Through Inhibition of Superoxide Formation.
    Date March 2006
    Journal Diabetes

    Statins may have favorable effects on endothelial barrier function, possibly through reduction of oxidative stress and modulation of expression of vasoactive proteins. The permeability of human umbilical endothelial cells in culture to a group of fluorescein isothiocyanate dextrans of different molecular weights were studied under various experimental conditions. Superoxide anion production was measured with an ethidium bromide fluorescence method. Cellular endothelin 1 mRNA and endothelin 1 in culture media were measured with Northern blots and enzyme immunoassays, respectively. Rosuvastatin (10 nmol/l) normalized the 500 mg/dl dextrose-induced permeability changes. Superoxide anion production induced by 500 mg/dl dextrose was inhibited by therapeutic concentrations of rosuvastatin or simvastatin (10 nmol/l), whereas the increased levels of cellular endothelin 1 mRNA and endothelin 1 in culture media was inhibited by supratherapeutic concentrations of statins (> or =0.1 micromol/l). In conclusion, 1) endothelial cell barrier dysfunction occurs in cells treated with high concentrations of dextrose, 2) statin treatment of endothelial cells normalizes barrier permeability, and 3) the favorable effects of statins may be attributed to the inhibition of the dextrose-induced increase in superoxide anions, whereas inhibition of endothelin expression was observed only at supratherapeutic concentrations.

    Title The Outcome of Cervical Exploration for Asymptomatic and Symptomatic Patients with Primary Hyperparathyroidism.
    Date March 2006
    Journal World Journal of Surgery

    This study examined the success and safety of cervical exploration in patients with primary hyperparathyroidism (HPT). The presentation, pathologic findings, and outcome of patients with asymptomatic primary HPT were compared with those with symptomatic disease. Records of patients undergoing cervical exploration for primary HPT from January 1993 until December 31, 2003, were reviewed. Information collected consisted of preoperative symptoms, calcium and parathormone (PTH) levels, imaging studies, operative findings, pathology, and outcome of the patients. The groups with asymptomatic and symptomatic primary HPT were compared. In all, 139 patients were studied; 31 (22.3%) were asymptomatic (group I), and 108 (77.7%) had symptoms (group II). The two groups were also comparable regarding mean age, sex, and the yield of the imaging studies. The mean preoperative serum calcium level was comparable in the two groups (11.1 mg/dl versus 11.3 mg/dl). However, PTH levels were significantly lower in group I than in group II (142 pg/dl versus 283 pg/dl, P = 0.01). The weight of the adenoma was also significantly less in group I than in group II (1082 mg versus 1679 mg P = 0.079). The outcome of the surgical exploration was comparable in the two groups with an immediate success rate close to 98% and a long-term success rate of 95.4%. Cervical exploration and parathyroidectomy in patients with primary HPT is a safe procedure with a high success rate and favorable outcome.

    Title Management of Obesity in the Elderly: Special Considerations.
    Date May 2005
    Journal Treatments in Endocrinology

    Over the last few decades, there has been an unprecedented increase in the prevalence of obesity, especially in economically developed countries. Furthermore, it is becoming an increasingly recognized health problem in the elderly. The precise mechanisms underlying increased adiposity in the elderly are not known. Aging is associated with a host of biologic changes that limit the ability of the individual to regulate energy homeostasis. Thus, it is likely that older individuals may be more likely to develop the two extremes of the spectrum of nutritional abnormalities, namely malnutrition and increased adiposity. These nutritional abnormalities are associated with significant morbidity and mortality. Current guidelines define overweight as a body mass index (BMI) of 25-29.9 kg/m2 and obesity as a BMI of 30 kg/m2 or more. However, the optimal BMI may be different in older individuals. Management strategies should attempt to optimize the nutritional status of older individuals. Age per se cannot be used as a justification for denying medical management of obesity to elderly individuals. Individualized programs with the goal of achieving modest weight reduction in obese patients are likely to result in immediate (e.g. alleviation of arthritic pains and reduction of glucose intolerance) and possibly long-term (e.g. reduction in cardiovascular risk) healthcare benefits. Management should emphasize lifestyle modifications, while the use of pharmacologic agents such as sibutramine and orlistat should be reserved for select groups of patients who do not respond to lifestyle modification.

    Title Rapid Adaptive Down Regulation of Oxidative Burst Induced by High Dextrose in Human Umbilical Vein Endothelial Cells.
    Date April 2005
    Journal Diabetes Research and Clinical Practice

    To determine whether hyperglycemia-induced increase in oxidative burst undergoes adaptive changes, the time course of superoxide (SO) production in human umbilical vein endothelial cells treated with 13.75 mM (D250) or 27.5mM dextrose (D500) was measured using the hydroethidine (HE) fluorescence method. The rate of SO production (mean +/- S.D., in arbitrary units) in cells treated with D500 during the first hour (0.758 +/- 0.367) or with D250 (0.618 +/- 0.126) was significantly higher than the rate observed in control cells treated with 100mg/dl dextrose, (D100; 0.474 +/- 0.125) (P < 0.001). However, the rate of SO production during the second, third, fourth, and fifth hour was not significantly different from that measured in control cells. The fluorescence at baseline for control cells was 3.4 +/- 2.3 and for cells treated with D500 for 1, 2, 3, 4, and 5h was 3.4 +/- 1.9, 15.2 +/- 2.5, 21.6 +/- 2.3, 27.4 +/- 3.4, and 31.8 +/- 4.3 respectively (P < 0.001). The increased baseline fluorescence suggests that the antioxidant pool may be depleted within the first hour of exposure to high concentrations of dextrose. The latter possibility is supported by the observation that treatment of cells with varying concentrations of ascorbate (15, 150, and 1500 microM) or alpha-tocopherol (10,100 and 1000 microM) prevents D500 induced increase in SO production. It is concluded that increased oxidative load in sustained chronic hyperglycemia is probably the result of depletion of antioxidant pool rather than secondary to sustained increase in SO production.

    Title Home Hospitalization Service for Acute Uncomplicated First Ischemic Stroke in Elderly Patients.
    Date December 2004
    Journal Journal of the American Medical Directors Association
    Title Hormonal Fountains of Youth.
    Date November 2004
    Journal Clinics in Geriatric Medicine

    Any hope of a fountain of youth to stop people from getting older is a long way off, with science just beginning to understand the complex genetic, physical, and hormonal causes of aging. Clearly, modem research has demonstrated that the concept of a hormonal fountain of youth is predominantly mythology. The best evidence supporting use of hormonal replacement is vitamin D and estrogen replacement to prevent hip fractures. Other than that, treatment should be limited to hormone replacement in persons who have endocrine disease.

    Title Induction of the Apolipoprotein Ai Promoter by Sp1 is Repressed by Saturated Fatty Acids.
    Date November 2004
    Journal Metabolism: Clinical and Experimental

    Insulin induces transcription of the hepatic apolipoprotein AI (apo AI) gene by increasing Sp1 binding to the promoter. To determine the effect of fatty acids on this process, HepG2 cells cotransfected with the plasmid pAI.474.CAT containing the full-length apo AI promoter and the Sp1-expressing plasmid, pCMV-Sp1, were studied. Chloramphenicol acetyl transferase (CAT) activity (% acetylation) increased 1.98-fold in cells receiving the Sp1 expression construct relative to control cells (46.4% +/- 0.6% v 23.4% +/- 1.3%, P < .05). Treatment of cells with 3 saturated fatty acids, stearic, myristic, and palmitic acid, repressed the ability of exogenous Sp1 to induce apo AI reporter gene expression (15.2% +/- 1.7%, 22.5% +/- 0.3%, 22.9% +/- 0.1%, 23.5% +/- 0.8%, respectively, P < .05). Unsaturated fatty acids, oleic, linoleic, or linolenic acid had no effect on Sp1-mediated induction of the apo AI promoter. In the presence of the trans fatty acids, CAT activity in the Sp1-transfected cells was similar to control cells (16.7% +/- 3.3%, 19.3% +/- 0.5%, and 21.0% +/- 2.1% acetylation in cells exposed to elaidic acid, linolelaidic, or linolenelaidic acid, respectively). In cells treated with an equimolar mixture of oleic acid and stearic acid, apo AI promoter activity was suppressed in a manner similar to that observed in stearic acid-treated cells. Insulin (100 microU/mL) induced apo AI promoter activity 2.9-fold (22.4% +/- 1.7% v 7.8% +/- 2.4%, P < .05). However, in the presence of stearic acid, insulin was unable to induce apo AI promoter (6.3% +/- 1.6%). Stearic acid treatment did not alter Sp1-DNA binding as measured by gel shift analysis. Therefore, saturated fatty acids blunt Sp1 induction of apo AI promoter probably at a step beyond DNA binding.

    Title Cyclooxygenase Inhibition is Associated with Downregulation of Apolipoprotein Ai Promoter Activity in Cultured Hepatoma Cell Line Hepg2.
    Date March 2004
    Journal Metabolism: Clinical and Experimental

    Prostanoids have been implicated in the transcriptional control of several genes. Since prostanoid synthesis inhibitors are commonly used in subjects with coronary heart disease we studied the effect of cyclooxygenase (COX) inhibition on apolipoprotein AI (apoAI) expression in a human hepatoma cell line (HepG2) transfected with full-length apoAI promoter attached to the chloramphenicol acetyl transferase (CAT) reporter gene. To control for transfection efficiency, the cells were cotransfected with the plasmid pCMV.SPORT-beta-gal containing the beta-galactosidase gene driven by the cytomegalovirus promoter. Treatment of these cells with varying concentrations of indomethacin (INDO, 0, 50, 100, and 300 micromol/L) resulted in a dose-dependent decrease in apoAI promoter activity (% acetylation corrected for beta-galactosidase activity: were 46.1 +/- 2.6, 29.9 +/- 1.2, 25.2 +/- 2.9, and 17.2 +/- 2.8, respectively, P <.001). INDO treatment did not cause significant changes in beta-galactosidase activity. A similar reduction in apoAI promoter activity was found after treating the cells with 50 micromol/L acetylsalicylic acid (ASA) (31.8 +/- 1.8%, P <.001), suggesting that the effect of INDO is related to COX inhibition rather than a peculiar effect of INDO. Nuclear run-off assays indicated that treatment of cells with 50 micromol/L INDO resulted in 31.4% reduction in apo A1 transcription rate (P <.0002). Northern blot analysis of RNA from HepG2 cells treated with 50 micromol/L of INDO for 72 hours showed that the apoAI mRNA concentration relative to G3PDH mRNA was 4,043.0 +/- 84.6 and 3,064.0 +/- 49.8 in control and INDO-treated cells, respectively (P <.0006). Kinetic studies of apoAI mRNA in HepG2 cells indicated that the half-life of apoAI mRNA was not significantly altered with 50 micromol/L INDO treatment. Apo AI mRNA half-life was 25.3 hours in control cells and 26.9 hours in INDO-treated cells. Western blot analysis of culture media of HepG2 cells treated with 50 micromol/L of INDO for 72 hours showed a significant reduction in apoAI protein (6,760.0 +/- 318.1 v 4,773.0 +/- 112.0 arbitrary units, P <.004). Treatment of cells with either arachidonic acid (COX substrate) or various prostanoids including prostaglandin I(2), thromboxane B(2), (+/-)5-HETE, or (+/-)12-HETE did not significantly alter apoAI promoter activity. However, prostaglandin E(1) and E(2) at the highest concentration tested (50 nmol/L) significantly repressed apoAI promoter activity. COX activity measurements in HepG2 cells verified the efficacy of COX inhibition by INDO. It is concluded that COX inhibition with INDO or ASA downregulates apoAI expression at the transcriptional level. This effect could not be attributed to either arachidonic acid excess or to a deficiency in various prostanoids tested.

    Title Effect of Chromium on Apolipoprotein A-i Expression in Hepg2 Cells.
    Date October 2003
    Journal Nutrition (burbank, Los Angeles County, Calif.)

    OBJECTIVE: Chromium is a key micronutrient required for lipid and carbohydrate metabolism. Some but not all clinical trials have associated use of chromium supplements with improved insulin sensitivity and lipid profile including increased high-density lipoprotein cholesterol levels. METHODS: Because apolipoprotein A-I (apoA-I) is the principal protein of high-density lipoprotein, the molecular pathways underlying chromium-related changes in apoA-I expression were studied in a human hepatoma cell line (HepG2) transfected with full-length apoA-I promoter attached to the reporter chloramphenicol acetyl transferase gene. RESULTS: Exposure of these cells to different concentrations of chromium chloride (0, 0.5, 1.0, and 3.0 mM) resulted in a dose-dependent decrease in apoA-I promoter activity (chloramphenicol acetyl transferase activity expressed as a percentage of an internal control was 99.4 +/- 7.2% in control cells versus 87.6 +/- 5.0%, 73.4 +/- 2.3%, and 36.6 +/- 3.9%, respectively, P < 0.01). Chromium chloride at 10 mM concentration was toxic and caused death in a large number of cells. Treating HepG2 cells with other minerals known to have insulin-sensitizing effects such as magnesium (1 mM), zinc (0.2 mM), and vanadyl sulfate (0.1 mM) significantly reduced apoA-I promoter activity in the presence and absence of 100 microU/mL of insulin. Northern blot analyses showed that the apoA-I mRNA content of cells treated with 0.2 mM of chromium chloride relative to G3PDH mRNA was not significantly increased compared with controls (0.652 +/- 0.122 versus 0.745 +/- 0.143, the ratio of apoA-I to glyceraldehyde 3-phosphate dehydrogenase (G3PDH) mRNA in control and chromium-treated cells, respectively). Western blot analyses of proteins secreted in culture media indicated that neither chromium treatment of the HepG2 cells (858.0 +/- 151.4 arbitrary units) nor treatment with magnesium (1323.3 +/- 175.7) or vanadium (1102 +/- 78.7) significantly altered apoA-I concentrations compared with controls (1061.7 +/- 114.7). However treatment of HepG2 cells with 0.2 mM of zinc significantly reduced apoA-I concentrations (291.0 +/- 29.2 versus 1061.7 +/- 114.7; P < 0.001). CONCLUSIONS: Supraphysiologic concentrations of chromium and other minerals with known insulin-sensitizing activity may reduce apoA-I promoter activity in cultured cells. Whether similar changes may occur in vivo remains to be shown. However, these observations do not support the use of pharmacologic amounts of chromium supplementation to enhance the cardioprotective lipid profile.

    Title Effect of Diabetes on the Blood Brain Barrier.
    Date June 2003
    Journal Current Pharmaceutical Design

    Diabetes mellitus is a metabolic disorder associated with structural and functional alteration of various organ systems including the central nervous system. The overall evidence suggests that the effect of Diabetes mellitus on the brain, although more subtle than some other chronic diabetic complications, is appreciable. A variety of pathogenetic mechanisms contribute to the central nervous system dysfunction in diabetic patient population. One major contributor is the Diabetes related alterations in the function of the blood-brain barrier (BBB). These alterations can be found in both barrier and transport components of the BBB function and can be attributed to changes in physicochemical properties of the endothelial cell membranes and of the tight junctions of the cerebral microvasculature. The present communication briefly reviews the Diabetes-related changes in the central nervous system and discusses some of the mechanisms underlying these changes.

    Title Effects of Dehydroepiandrosterone on Rat Apolipoprotein Ai Gene Expression in the Human Hepatoma Cell Line, Hepg2.
    Date March 2002
    Journal Metabolism: Clinical and Experimental

    Serum apolipoprotein AI (apoAI) levels correlate with the risk of developing atherosclerosis. Previous studies have suggested that dehydroepiandrosterone (DHEA) lowers high-density lipoprotein (HDL)-cholesterol levels. We investigated whether or not DHEA may lower HDL-cholesterol levels by suppressing apoAI gene transcription in hepatocytes. ApoAI mRNA levels, assessed by Northern blotting, were suppressed in HepG2 cells treated with DHEA (34%) (10 microg/mL) or testosterone (36%) (T, 1 microg/mL). Estradiol alone (E2, 1 microg/mL) had relatively little effect on apoAI mRNA levels, while E2 in combination with DHEA prevented a decrease in apoAI mRNA levels compared to DHEA alone. To determine whether these effects were due to changes in apoAI gene transcription, HepG2 cells were transfected with a plasmid carrying the full-length promoter of the rat apoAI gene ligated into a chloramphenicol acetyltransferase (CAT) reporter construct. The plasmid pCMV.SPORT-beta-gal was included in each transfection to normalize the data to transfection efficiency. Cells were then cultured in the presence or absence of DHEA (10 microg/mL), T (1 microg/mL), 17alpha-methyltestosterone (MTT, 1 microg/mL), 5alpha-dihydrotestosterone (DHT, 1 microg/mL), E2 (1 microg/mL), or a combination of DHEA plus E2, T plus E2, MTT plus E2, and DHT plus E2, for 24 hours. CAT activity, relative to beta-galactosidase activity, was reduced by 19.6%, 57.6%, 38.6%, and 54.6% with DHEA, T, DHT, and MTT addition, respectively. E2 increased CAT activity by 43.8%. When the androgens (ie, DHEA, T, DHT, or MTT) were combined with E2, apoAI promoter activity was suppressed. We conclude, therefore, that androgens downregulate apoAI promoter activity in the presence or absence of E2. However, the changes in mRNA levels do not always reflect changes in promoter activity, suggesting that these steroids may have additional post-transcriptional effects on steady-state apoAI mRNA levels. It remains to be established if the transcriptional effects we observed are mediated through an androgen response element.

    Title Seroprevalence of Viral Hepatitis in an Older Nursing Home Population.
    Date September 1999
    Journal Journal of the American Geriatrics Society

    OBJECTIVES: To assess the prevalence of current or previous infection with viral hepatitis agents in an older nursing home population. DESIGN: A prospective cohort study. SETTING: Three nursing homes in the greater St. Louis area affiliated with Saint Louis University. SUBJECTS: Older residents admitted to these facilities. MEASUREMENTS: Residents were interviewed and examined for evidence of hepatitis or liver disease. Serum samples were tested for hepatitis B surface antigen (HBsAg), antibody to hepatitis B core and surface antigens (anti-HBc and anti-HBs), antibody to hepatitis A virus (anti-HAV), antibody to hepatitis C virus (anti-HCV), and hepatitis G virus RNA (HGV RNA). RESULTS: Of 329 residents queried, 199 gave consent and were able to participate. The seroprevalence of hepatitis was: HBsAg 0%, anti-HBc 24.1%, anti-HBs 19.5%, anti-HAV 79.9%, anti-HCV 4.5%, and HGV-RNA 10.6%. Frequency of HAV infection increased significantly with age whereas HBV infection correlated with ethnic status and former occupation as a manual worker. A history of blood transfusion was associated with a higher rate of anti-HCV. End stage renal disease, present in 17 patients, was associated with anti-HBc, anti-HCV, and HGV RNA positivity but not with anti-HBs or anti-HAV positivity CONCLUSIONS: The seroprevalence of anti-HCV was surprisingly high in this population residing in skilled nursing facilities, and we recommend that all new patients admitted to this type of institution be screened for anti-HCV. The prevalence of HGV RNA was higher than in the general US blood donor population, but the significance of this finding remains uncertain.

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