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Biomedical subjects

Raj Vuppalanchi

Publications and source records attributed to Raj Vuppalanchi.

6 recordsLinked to original sources
PubMed2006

Glycosylphosphatidylinositol-specific phospholipase d in nonalcoholic Fatty liver disease: a preliminary study.

CONTEXT: Recent studies demonstrated that de novo lipogenesis is increased in patients with nonalcoholic fatty liver disease (NAFLD). Patients with NAFLD also have plasma lipid abnormalities. These lipid abnormalities may in part be related to insulin resistance, which is common in patients with NAFLD. Insulin resistance is associated with alterations in proteins involved in lipid metabolism including glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD), which is involved in triglyceride metabolism. OBJECTIVE: The objective of the study was to determine whether alterations in serum and hepatic levels of GPI-PLD occur in patients with NAFLD. DESIGN AND PATIENTS: We examined the following: 1) levels of serum GPI-PLD in nondiabetics with nonalcoholic steatohepatitis, compared with matched controls; 2) hepatic expression of GPI-PLD mRNA in patients with normal liver or NAFLD; and 3) effect of overexpressing GPI-PLD vs. beta-galactosidase (control) on global gene expression in a human hepatoma cell line. RESULTS: The serum levels of GPI-PLD were significantly higher in patients with nonalcoholic steatohepatitis than in matched controls (119 +/- 24 vs.105 +/- 15 microg/ml, P = 0.047). The hepatic expression of GPI-PLD mRNA was increased nearly 3-fold in NAFLD patients, compared with patients with normal liver (3.1 +/- 2.6 vs. 1.1 +/- 1.0 arbitrary units per microgram total RNA, P = 0.026). Finally, overexpressing GPI-PLD was associated with an increase in de novo lipogenesis genes. CONCLUSIONS: Patients with NAFLD have elevated serum levels and hepatic expression of GPI-PLD, and its overexpression in vitro is associated with increased expression of de novo lipogenesis genes. These results suggest that GPI-PLD may play a role in the pathogenesis of NAFLD and/or its metabolic features and warrants further investigation.

Adult↗
PubMed2005

Patients with elevated baseline liver enzymes do not have higher frequency of hepatotoxicity from lovastatin than those with normal baseline liver enzymes.

BACKGROUND: It is recommended that lovastatin be avoided in patients with unexplained elevation in transaminase levels. However, there are no studies that evaluated the risk of lovastatin hepatotoxicity in subjects with elevated liver enzymes. Our study tested the hypothesis that patients with elevated liver enzymes are not at higher risk for hepatotoxicity from lovastatin. METHODS: Our study consisted of the following three cohorts of patients seen between December 1987 and December 1998: cohort 1: 135 patients with elevated baseline enzymes (aspartate transaminase [AST] >40 IU/L or alanine transaminase [ALT] >35 IU/L) who received lovastatin; cohort 2: 620 patients without elevated liver enzymes who received lovastatin; and cohort 3: 2644 patients with elevated liver enzymes but not prescribed lovastatin. Elevations in liver biochemistries over a 12-month period after lovastatin was prescribed were categorized into mild-moderate or severe elevations and into "Hy's Rule" based on published criteria. RESULTS: The incidence of mild-moderate elevations and severe elevations in liver biochemistries in cohort 1 were 6.6% and 0%, respectively. Compared with cohort 2, individuals in cohort 1 had higher incidence of mild-moderate elevations (6.6% versus 3%; P = 0.03) but not severe elevations (0% versus 0.3%; P = 0.9). Compared with cohort 3, patients in cohort 1 had similar mild-moderate elevations (6.6% versus 11%; P = 0.2) but lower severe elevations (0% versus 5.5%; P < 0.01). No one in cohorts 1 or 2 developed elevations meeting Hy's Rule, whereas 3.5% of the patients in cohort 3 exhibited such elevations (P < 0.05 versus cohort 1 or cohort 2). CONCLUSIONS: Significant hepatotoxicity from lovastatin was very infrequent in this study, and individuals with elevated baseline liver enzyme levels did not have higher frequency of lovastatin hepatotoxicity than those with normal liver enzyme levels.

Adult↗
PubMed2005

Is adiponectin involved in the pathogenesis of nonalcoholic steatohepatitis? A preliminary human study.

BACKGROUND: Animal studies have suggested that adiponectin may play a role in the pathogenesis of alcoholic and nonalcoholic fatty liver disease. Studies are limited that evaluated the role of adiponectin in the pathogenesis of nonalcoholic steatohepatitis (NASH). METHODS: To further our understanding of the role of adiponectin in the pathogenesis of NASH, the following studies were conducted. Serum adiponectin was measured and correlated with anthropometric and nutritional variables in 21 patients with biopsy-proven NASH and 19 age-, gender-, body mass index-, and body fat-matched controls. The effect of a mixed meal on serum adiponectin levels in a subgroup of patients (n = 24) with NASH and controls was assessed. In a separate cohort, liver samples belonging to healthy (n = 11), steatotic (n = 12), and NASH (n = 12) patients were used to further explore the role of adiponectin by measuring the expression of adiponectin and adiponectin receptor (AdipoR2) mRNA. RESULTS: Patients with NASH had significantly lower levels of serum adiponectin than controls (4.9 +/- 2.7 vs. 7.3 +/- 3.5 microg/mL, P = 0.02). While no significant correlation existed between serum adiponectin and anthropometric or nutritional variables, it was independently associated with age, high density lipoprotein, and triglycerides. Mixed meal had no effect on serum adiponectin either in patients with NASH or in controls. There was no expression of adiponectin mRNA in any of liver samples studied. However, AdipoR2 mRNA expression was higher in NASH than in steatotic and normal liver tissue. CONCLUSION: These data show that adiponectin may have a role in the pathogenesis of human NASH and should be investigated further.

Adiponectin↗
PubMed2005

Interrelationship between thyroid nodularity and TSH level.

BACKGROUND: The pathophysiological role of thyroid-stimulating hormone (TSH) in the development of goiter is controversial. The aim of this study was to examine the relationship between thyroid nodularity and serum TSH levels in clinically and biochemically euthyroid patients with non-endemic multinodular goiter. METHODS: We surveyed 44 of our endocrine clinic patients with multinodular goiter. Twenty-five patients with suppressed TSH levels or positive antithyroid antibodies were excluded. The remaining 19 patients were included (group 1). The 19 study subjects were compared with 19 age- and sex- matched controls without any thyroid disease or goiter (group 2). TSH levels in both groups were checked by review of their medical records. RESULTS: In group 1, TSH ranged from 0.68-3.68 IU/mL (normal: 0.4-6.0 IU/mL), with a mean of 1.45 +/- 0.29. In group 2, TSH ranged from 0.38-1.88 IU/mL, with a mean of 1.08 +/- 0.1. The differences of these values, analyzed by paired t test (p=0.22), were not statistically significant. CONCLUSIONS: These data suggest that TSH levels in euthyroid patients with multinodular goiter are not significantly different from those in normal controls.

Case-Control Studies↗