A5101539133- Peroxisome Proliferator-Activated Receptors
- Adipose Tissue and Metabolism
- Adipokines, Inflammation, and Metabolic Diseases
- Liver Disease Diagnosis and Treatment
- Immune Response and Inflammation
- Diet and metabolism studies
- Metabolism and Genetic Disorders
- Fatty Acid Research and Health
- Drug Transport and Resistance Mechanisms
- Appendicitis Diagnosis and Management
- Sphingolipid Metabolism and Signaling
- Mitochondrial Function and Pathology
- Metabolism, Diabetes, and Cancer
- Metabolomics and Mass Spectrometry Studies
- Weed Control and Herbicide Applications
- Natural Language Processing Techniques
- Diabetes, Cardiovascular Risks, and Lipoproteins
- Lipid metabolism and disorders
- Pancreatic function and diabetes
- Glioma Diagnosis and Treatment
- Cholesterol and Lipid Metabolism
- Cardiac, Anesthesia and Surgical Outcomes
- Seed Germination and Physiology
- Paraoxonase enzyme and polymorphisms
- Infectious Diseases and Tuberculosis
University of Sindh
2006-2024
Bilawal Medical College
2024
Liaquat University of Medical & Health Sciences
2015-2024
Namal College
2024
Baqai Institute of Diabetology and Endocrinology
2024
Lahore University of Management Sciences
2021
Children's Mercy Hospital
2018
San Francisco VA Medical Center
1993-2015
Aga Khan University
1995-2009
Boston University
2009
Peroxisome proliferator-activated receptors (PPARs) are transcription factors that play an important role in the regulation of genes involved lipid utilization and storage, lipoprotein metabolism, adipocyte differentiation, insulin action. The three isoforms PPAR family, i.e. α, δ, γ, have distinct tissue distribution patterns. PPAR-α is predominantly present liver, PPAR-γ adipose tissue, whereas PPAR-δ ubiquitously expressed. A recent study reported increased messenger RNA (mRNA) expression...
Abstract —Epidemiological studies have shown an increased incidence of coronary artery disease in patients with chronic infections and inflammatory disorders. Because oxidative modification lipoproteins plays a major role atherosclerosis, the present study was designed to test hypothesis that host response infection inflammation induces lipoprotein oxidation vivo. Lipoprotein measured 3 distinct models inflammation. Syrian hamsters were injected bacterial lipopolysaccharide (LPS), zymosan,...
The host response to infection is frequently accompanied by changes in cholesterol and triglyceride (TG) metabolism. To determine the role of cytokines mediating these changes, we studied effects endotoxin (LPS), tumor necrosis factor-alpha (TNF) interleukin-1 beta (IL-1) on TG metabolism C57Bl/6 (LPS-sensitive) mice C3H/HeJ (LPS-resistant) whose macrophages do not produce TNF IL-1 LPS. Sixteen hours after administration, LPS (1 micrograms/mouse) produced a 41% increase serum 62% levels...
Infection and inflammation increase serum triglyceride cholesterol levels in rodents rabbits.Endotoxin (LPS) has been used as a model of infection its effects on metabolism have previously characterized.In the present study we demonstrate that both low (100 ng/100 g body weight) high dose pg/lOO LPS hamsters.The is first observed 16 h after persists for at least 24 h.This primarily due to an density lipoprotein (LDL) cholesterol.High (HDL) decrease treatment.Both hepatic synthesis (low 85%,...
Abstract —Alterations in triglyceride and cholesterol metabolism often accompany inflammatory diseases infections. We studied the effects of endotoxin (lipopolysaccharide [LPS]) cytokines on hepatic sphingolipid synthesis, activity serine palmitoyltransferase (SPT), first rate-limiting enzyme lipoprotein content Syrian hamsters. Administration LPS induced a 2-fold increase SPT activity. The occurred at 16 hours, peaked 24 was sustained for least 48 hours. Low doses produced maximal increases...
The cloning of two novel fatty acid (FA) transport proteins, FA protein (FATP) and translocase (FAT), has recently been reported; however, little is known about their in vivo regulation. Endotoxin [lipopolysaccharide (LPS)], tumor necrosis factor (TNF), interleukin-1 (IL-1) stimulate adipose tissue lipolysis enhance hepatic lipogenesis reesterification while suppressing oxidation multiple tissues. Hence, this study we examined effects on FATP FAT mRNA levels Syrian hamsters. Our results...
Introduction Initiated in June 2019, this collaborative effort involved 15 public and private sector hospitals Pakistan. The primary objective was to enhance the capacity for pediatric neuro-oncology (PNO) care, supported by a My Child Matters/Foundation S grant. Methods We aimed establish operate Multidisciplinary Tumor Boards (MTBs) on national scale, covering 76% of population (185.7 million people). In response COVID-19 pandemic, MTBs transitioned videoconferencing. Fifteen with...
The hyperlipidemia associated with obesity and type 2 diabetes is caused by an increase in hepatic triglyceride synthesis secretion that secondary to de novo lipogenesis, a decrease fatty acid (FA) oxidation, the flux of peripherally derived FA liver. uptake across plasma membrane may be mediated three distinct proteins--FA translocase (FAT), binding protein (FABP-pm), transport (FATP)--that have recently been characterized. Acyl-CoA synthetase (ACS) enhances FAs catalyzing their activation...
The host response to infection is associated with several alterations in lipid metabolism that promote lipoprotein production. These changes can be reproduced by lipopolysaccharide (LPS) administration. LPS stimulates hepatic cholesterol synthesis and suppresses the conversion of bile acids. down-regulates 7α-hydroxylase, rate-limiting enzyme classic pathway acid synthesis. We now demonstrate markedly decreases activity sterol 27-hydroxylase, alternate synthesis, liver Syrian hamsters....
To determine the role of cytokines in mediating decrease ketones associated with infection, we studied effect endotoxin (LPS), interleukin-1 (IL-1), and tumor necrosis factor (TNF) on serum hepatic ketone body levels (KB), free fatty acids (FFA), malonyl-CoA levels. LPS decreased KB C57Bl/6 (LPS sensitive) mice, whereas it had little C3H/HeJ resistant) whose macrophages lack ability to produce IL-1 TNF response LPS, suggesting that may mediate this effect. both strains mice. As seen KB, no...
The host response to infection is frequently accompanied by changes in cholesterol and triglyceride (TG) metabolism. To determine the role of cytokines mediating these changes, we studied effects endotoxin (LPS), tumor necrosis factor-alpha (TNF) interleukin-1 beta (IL-1) on TG metabolism C57Bl/6 (LPS-sensitive) mice C3H/HeJ (LPS-resistant) whose macrophages do not produce TNF IL-1 LPS. Sixteen hours after administration, LPS (1 micrograms/mouse) produced a 41% increase serum 62% levels...
Acyl-CoA synthetase (ACS) catalyzes the activation of fatty acids (FA) to acyl-CoA esters, which are further metabolized in either anabolic or catabolic pathways. Endotoxin [lipopolysaccharide (LPS)], tumor necrosis factor (TNF), and interleukin-1 (IL-1) enhance hepatic FA synthesis reesterification inhibit oxidation. LPS also decreases triglyceride storage adipose tissue inhibits uptake by heart muscle. Therefore, this study we examined effects cytokines on ACS (now known as ACS1) mRNA...
Plasma platelet-activating factor acetylhydrolase (PAF-AH) hydrolyzes PAF and oxidized phospholipids is associated with lipoproteins in the circulation. Endotoxin [lipopolysaccharide (LPS)], a potent inducer of acute phase response (APR), produces marked changes several proteins that play important roles lipoprotein metabolism. We now demonstrate LPS 2.5- to 3-fold increase plasma PAF-AH activity Syrian hamsters. The found high-density (HDL) fraction increased threefold treatment despite...
The host response to infection is associated with multiple alterations in lipid and lipoprotein metabolism. We have shown recently that endotoxin (lipopolysaccharide (LPS)) cytokines enhance hepatic sphingolipid synthesis, increase the activity mRNA levels of serine palmitoyltransferase, first committed step content sphingomyelin, ceramide, glucosylceramide (GlcCer) circulating lipoproteins Syrian hamsters. Since LPS-induced GlcCer was far greater than ceramide or we now examined effect LPS...
The host response to infection and inflammation is associated with multiple alterations in lipid metabolism. We have shown that endotoxin [lipopolysaccharide (LPS)] stimulates hepatic sphingolipid synthesis increases ceramide glucosylceramide (GlcCer) content circulating lipoproteins Syrian hamsters. LPS also the activity mRNA levels of serine palmitoyltransferase (SPT) GlcCer synthase, committed enzymes glycosphingolipid (GSL) synthesis, respectively, liver. To determine whether GSL...
The host response to infection and cancer produces disturbances in fatty acid (FA) oxidation ketogenesis. Interferons (IFNs) stimulate lipolysis cultured adipocytes. Since FA mobilization is a major stimulus for ketogenesis, we studied the effect of IFN alpha gamma on ketogenesis intact mice. Both IFNs acutely stimulated lipolysis; however, their effects differed. INF increased serum hepatic ketone body levels parallel its FFA, whereas exerted biphasic At low doses, levels, at higher this...