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Hepatocellular carcinoma is a prevalent form of liver cancer that is life threatening. Many chemically synthesized anti-cancer drugs have various degrees of side effects. Hence, this study investigated the effect of FEAC interventions on NDEA-CCl4-induced HCAR in male Wistar rats. HCAR was induced by intraperitoneal administration of 200 mg/kg of NDEA and 0.5 mL/kg CCl4 (as a promoter of HCAR). Following the induction of HCAR, rats were treated differently with two different doses (25 and 50 mg/kg) of FEAC. HCAR induction was confirmed by the significant elevation of serum levels of ALT, AST, and α-FP. Also elevated significantly were liver levels of Akt/PKB, NF-κB, TNF-α, MDA, GSH, and activities of GST, SOD, and CAT, while levels of liver p53 and Nrf2 were significantly lowered compared with normal rats. Treatment interventions with both 25 and 50 mg/kg of FEAC against the DEN-CCl4-induced HCAR gave comparable effects, marked by a significant reduction in the levels of serum ALT, AST and α-FP, as well as liver levels of MDA, GSH, Akt/PKB, NF-κB, TNF-α, GST, SOD, and CAT, while levels of liver p53 and Nrf2 were significantly elevated compared with normal rats. Put together and judging by the outcomes of this study, FEAC being a potent antioxidant may also be potent against chemical-induced HCAR via upregulation of p53 and Nrf2, as well as downregulation of the Akt/PKB-NF-κB pathway in rats.

Background: Ferulic acid (FAC) is a component of plant cell walls, where it serves as a building block of lignin and pectin. As such, it is abundantly found in vegetables and other plants. In contrast, 2-methoxyethanol (2METH) is a testicular toxin commonly found in products used by humans. This study is aimed to investigate the effect of FAC on 2METH-induced testicular inflammation in rats. Method: Four groups of 5 animals each were used: Group I served as the control, Group II was exposed to 2METH only (100 mg/kg), Group III was administered 2METH (100 mg/kg) plus FAC (50 mg/kg), and Group IV served as the FAC (50 mg/kg) only group. All administrations were done orally for 30 days. Results: At the end of the study, rats administered 2METH only showed a significant increase in the testicular levels of interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-α), inducible nitric oxide synthase (iNOS), cyclooxygenase 2 (COX-2), and nuclear factor κB (NF-κB), as well as RNA gene expressions of Janus kinase 1 (JAK1), signal transducer and activator of transcription 1 (STAT1), and suppressor of cytokine signaling 1 (SOCS1) compared to the control group. In contrast, treatment with FAC led to a significant decrease in the testicular levels of IL-6, TNF-α, iNOS, COX-2, NF-κB, and gene expression of STAT1, while significantly increasing the testicular gene expression of protein inhibitor of activated STAT 1 (PIAS1) compared to rats exposed to 2METH only. Conclusion: Based on the data gathered from this study, FAC demonstrated an anti-inflammatory effect by inhibiting the testicular activation of NF-κB through the downregulation of pro-inflammatory markers (IL-6, TNF-α, iNOS, and COX-2) and the inhibition of the STAT1-PIAS1 signaling pathway in rats.

Dimethyl nitrosamine (DMN) is a known hepatotoxin, carcinogen, and mutagen. This study is therefore carried out to investigate the therapeutic effects of syringic acid (SYRA) and ascorbic acid (ASCA) in DMN-induced hepatic injury in rats. Following DMN administrations, malondialdehyde (MDA), nitric oxide (NO) and reduced glutathione (GSH) as well as activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) were significantly increased. Also significantly increased were levels of tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). Following treatment with SYRA and ASCA, the activities of ALT, AST, GPx, CAT and SOD, as well as MDA, GSH, TNF-α, IL-1β, and NFkB levels were significantly reduced. Overall, both treatments were effective, but SYRA had a better therapeutic effect than ASCA. Therefore, this promising potential of SYRA can be taken advantage of in the treatment of DMN-induced hepatic injury.

Ulcerative colitis is an idiopathic disease attributed to an aggressive dysregulated immune response that results in epithelial injury and diffuse inflammation in the colon. Ulcerative colitis may be acute or chronic with unpredictable relapse. Kolaviron, a bioflavonoid extracted from Garcinia kola has been reported to possess gastroprotective properties. We have previously reported the protective effect of kolaviron on acute colitis. This study investigated the effect of kolaviron on dextran sulphate sodium-induced chronic ulcerative colitis in Balb/c mice. Mice were randomly assigned to four groups of 10 mice each. Group I (Control) mice received corn oil at 2 ​ml/kg for forty-nine days. Group II mice received kolaviron at 200 ​mg/kg for forty-nine days. Group III mice received 3 cycles of dextran sulphate sodium (DSS) (2.5% w/v) in drinking water (each cycle is defined as 7 days of 2.5% DSS followed by 7 days of normal drinking water). Group IV received Kolaviron at 200 ​mg/kg body weight for 7 days before co-administration with 3 cycles of DSS (2.5% w/v). Administration of kolaviron significantly ameliorated increases in disease activity index in DSS-induced chronic ulcerative colitis in mice. Furthermore, kolaviron suppresses the expression of inducible nitric oxide synthase and cyclooxygenase-2 in DSS-treated mice. Additionally, kolaviron protected against colonic oxidant stress damage by augmenting the endogenous antioxidant with concomitant decrease in myeloperoxidase activity, tumor necrosis factor alpha, Interleukin-1β, and lipid peroxidation levels in DSS-treated mice. Moreover, kolaviron attenuated the disruption of the colonic histological architecture and reduced neutrophil infiltration in DSS-treated mice. In conclusion, kolaviron ameliorated DSS-induced chronic ulcerative colitis via antioxidant and anti-inflammatory mechanisms.

Asthma is a chronic non-communicable inflammatory disease of the lung that affects over 300 million people worldwide. 6-Gingerol (6-G) is a phytocompound found in ginger rhizome that has been reported to exhibit anti-inflammatory effects. However, there is paucity of information regarding the effect of 6-G on asthma. This study was designed to evaluate the effect of 6-G on house dust mite (HDM) -induced asthma. Male mice were divided into 5 groups of 10 mice each. Group 1 served as control; group 2 received 6-G (10 mg/kg/day) for 5 weeks. Group 3 received HDM (10 µg/kg/day) for 4 weeks. Group 4 received 6-G (10 mg/kg/day) for 1 week prior to co-exposure with HDM (10 µg/kg/day) for 4 weeks, and group 5 received Dexamethasone (DEX) (1 mg/kg/day) and HDM (10 µg/kg/day) for 4 weeks. Administration of HDM significantly increased lymphocytes, leukocytes, neutrophils, eosinophils, myeloperoxidase (MPO), nitric oxide (•NO), malondialdehyde, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and decreased the activities of superoxide dismutase (SOD), catalase, glutathione S-transferase (GST), glutathione peroxidase (GPx), glutathione (GSH) and ascorbic acid (AA) levels relative to control. Administration of 6-G and DEX prior to HDM exposure significantly decreased lymphocytes, leukocytes, neutrophils, eosinophils, MPO, •NO, malondialdehyde, TNF-α, IL-6 and increased the activities of SOD, catalase, GST, GPx, and levels of GSH and AA relative to HDM group. Histopathological examination of the lungs of HDM-treated mice showed the presence of oedema and inflammation of the bronchi and alveoli. Administration of 6-G and DEX reversed these lesions. 6-G ameliorated House dust mite-induced asthma via anti-inflammatory and anti-oxidant mechanism.

Idiopathic lung fibrosis (ILF) is a severe and life threatening lung disorder that is characterized by scarring of lung tissue, leading to thickening and stiffening of affected areas. This study looked at the role played by PI3K-Akt/PKB-mToR signaling pathway in the pathogenesis of N-Nitrosodimethylamine (NDMA)-induced lung fibrotic injury, and the effects of syringic acid (SYR) and ascorbic acid (ASC) treatments in male Wistar rats. Pulmonary fibrosis was induced by intraperitoneal injection of 10 mg/kg NDMA once daily, thrice (consecutively) a week for four weeks, and this condition was treated daily with SYR (50 mg/kg) and ASC (100 mg/kg) acids orally for four weeks. Fibrogenesis, following NDMA administration was marked by a significant increase in collagen-1 and α-SMA levels, while oxidative stress was marked by a significant decrease in GSH level, GST, GPx, CAT, and SOD activities. Also, NDMA significantly increased lung Bax, p53, caspase-3, TNF-α, IL-1β, NFkB, and decreased Bcl-2, mdm2, cyclin D1 and Nrf-2 levels. Looking at the PI3K-Akt-mTOR signaling pathway, NDMA administration significantly activated lung PI3K, Akt, and mTOR, and deactivated PTEN, FoxO1 and TSC2. Treatments with SYR and ASC significantly reduced oxidative stress by restoring the antioxidant systems via Nrf2 activation, decreased the levels of inflammatory markers through inhibition of NFkB, downregulated p53, Bax, and caspase-3 via up-regulation of mdm2 and cyclin D1. SYR and ASC also regulated the PI3K-Akt-mTOR signaling pathway via the deactivation of PI3K, Akt, and mTOR, and up-regulation of PTEN, FoxO1 and TSC2. Overall, SYR and ASC modulate the PI3K-Akt-mTOR signaling pathway via inhibition of oxidative stress, inflammation and apoptosis in NDMA-induced lung fibrosis.

Reproductive and neurological anomalies are often characterized by malfunctioning of reproductive and nervous organs sometimes attributed to systemic toxins. However, limited information is available on the impact of snake venom toxins on male reproductive and nervous system. This study investigated the toxicological effects of Naja nigricollis venom on male reproductive and neural functions in rat model. Twenty male Wistar rats weighing between 195 and 230 g were divided randomly into two groups of ten rats each. Group 1 served as normal control while rats in group 2 were envenomed with a single intraperitoneal injection of 0.25 mg/kg−1 (LD12.5) of N. nigricollis venom on first and twenty fifth day within the period of fifty days experiment. The venom significantly decreased sperm counts, motile cells and volume combined with increased sperm abnormalities. The venom induced hormonal imbalances in the envenomed group as levels of testosterone, luteinizing and follicle stimulating hormones depreciated compared to the control. Oxidative stress biomarkers: malondialdehyde significantly increased parallels with depletion of glutathione level and catalase activities in testis, epididymis and brain of envenomed rats. Furthermore, N. nigricollis venom up-regulated tumor necrosis factor-alpha (TNF-α) and interleukin1-beta (IL-1β) production in testis, epididymis and brain of envenomed rats compared to the control. Also, various histological alterations were noticed in tissues of testis, epididymis and brain of envenomed rats. Findings indicated that N. nigricollis venom is capable of inducing reproductive and neurological dysfunction in envenomed victims.

Methyl cellosolve (MC) is used in production of textile, paints, stains, inks, surface coatings, and anti-icing additive in hydraulic fluids and jet fuel. Consequently, the present study investigated its effect on renal cells, in a time-course study in male Wistar rats. Animals were orally administered 50 mg/kg body weight of MC for a period of 7, 14, and 21 days. Following 7 days of administration of MC, there was a significant increase in the levels of K-Ras, c-Myc, TNF-α, IL-6 and NO, while GSH level and SOD activity were significantly reduced compared with control. At the end of 14 days exposure, RKW, GSH, NO, and Bcl-2 levels were significantly decreased, while levels of K-Ras, c-Myc, p53, Bax, caspase-3, TNF-α, IL-1β, IL-6, MDA and GPx activity were significantly increased compared with control. After 21 days of MC administration, RKW, GSH, NO, IL-10 and Bcl-2 levels were significantly decreased, while levels of K-Ras, c-Myc, p53, Bax, caspase-3, TNF-α, IL-1β, IL-6, MDA and GST activity were significantly increased compared with control. Exposures to MC in any way should be strictly avoided as it could trigger renal damage through the disorganization of the antioxidant system, up-regulation of inflammatory, apoptotic, and oncogenic markers in rats.

The energy in wireless sensor networks is considered a scarce commodity, especially in scenarios where it is difficult or impossible to provide supplementary energy sources once the initially available energy is used up. Even in cases where energy harvesting is feasible, effective energy utilization is still a crucial step for prolonging the network lifetime. Enhancement of life-time through efficient energy management is one of the essential ingredients underlining the design of any credible wireless sensor network. In this paper, we propose a sensor selection method using a novel and unsupervised neural network structure referred to as partly-informed sparse autoencoder (PISAE) that aims to reconstruct all sensor readings from a select few. The PISAE comprises three submodules, namely: the gate (which selects the most important sensors), encoder (encodes and compresses the data from select sensors), and decoder (decodes the output of the encoder and regenerates the readings of all initial sensors). Our approach relies on the premise that many sensors are redundant because their readings are spatially and temporally correlated and are predictable from the readings of a few other sensors in the network. Thus, overall network reliability and lifetime are enhanced by putting sensors with redundant readings to sleep without losing significant information. We evaluate the efficacy of the proposed method on three benchmark datasets and compare with existing results. The experimental results indicate the superiority of our approach compared with existing approaches in terms of accuracy and lifetime extension factor.

Camphor-induced oxidative stress and histopathological changes (in brain, lung, liver, kidney and testes) have been reported. We therefore investigated the effect of various doses of camphor in an acute study, on renal and testicular levels of some pro-inflammatory mediators in male wistar rats. Twenty rats divided into four groups of five rats each were used in this study. Group 1 served as control and was administered 6 mL/kg olive oil, the vehicle for camphor, while groups 2, 3 and 4 were orally administered 1000, 2000, and 4000 mg/kg body weight camphor, for seven days. Compared with control, levels of tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β) and interleukin 6 (IL-6) were significantly increased kidney and testes by 2000 and 4000 mg/kg body weight, while interleukin 10 (IL-10) was only significantly increased by 1000 mg/kg body weight of camphor in both tissues. Also compared with control, all doses of camphor administered resulted in a significant increase in the expressions of renal and testicular nuclear factor kappa B (NFkB), cyclooxygenase 2 (COX-2), regulated upon activation normal T cell expressed and secreted (RANTES), and monocyte chemo-attractant protein 1 (MCP-1). Conclusively, use and consumption of camphor should be with caution as it could trigger renal and testicular inflammation through activation of NF-kB and up-regulation of pro-inflammatory markers. Keywords: Camphor, Chemokines, Cytokines, Pro-inflammation, Renal, Testicular

Naja haje envenoming could activate multiple pathways linked to haematotoxic, neurological, and antioxidant systems dysfunctions. Moringa oleifera has been used in the management of different snake venom-induced toxicities, but there is no scientific information on its antivenom effects against Naja haje. This study thus, investigated the antivenom activities of different extract partitions of M. oleifera leaves against N. haje envenoming. Forty five male rats were divided into nine groups (n = 5). Groups 2 to 9 were envenomed with 0.025 mg/kg (LD50) of N. haje venom while group 1 was given saline. Group 2 was left untreated, while group 3 was treated with polyvalent antivenom, groups 4, 6 and 8 were treated with 300 mg/kg−1 of N-hexane, ethylacetate and ethanol partitions of M. oleifera, respectively. Groups 5, 7 and 9 were also treated with 600 mgkg−1of the partitions, respectively. Ethanol extract and ethyl acetate partition of M. oleifera significantly improved haematological indices following acute anaemia induced by the venom. Likewise, haemorrhagic, haemolytic and anti-coagulant activities of N. haje venom were best inhibited by ethanol partition. Envenoming significantly down-regulated Nuclear factor erythroid 2-related factor 2 (Nrf2) with the consequent elevation of antioxidant enzymes activities in the serum and brain. Treatment with extract partitions however, elevated Nrf2 levels while normalising antioxidant enzyme activities. Furthermore, there were reduction in levels of pro-inflammatory cytokines (TNF-α and interleukin-1β) in tissues of treated envenomed rats. This study concludes that ethanol partition of M. oleifera was most effective against N. haje venom and could be considered as a potential source for antivenom metabolites.

This study examined the effect of co-administration of sodium selenite (SS) and sodium arsenite (SA) on inflammation in rats. Thirty (30) male Wistar rats were separated into 6 groups of five animals each. Group I (control) was given distilled water, groups II, III, IV and V were exposed to 20 and 40 ppm SA in drinking water, but in addition to that, groups IV and V only were co-exposed with 0.25 mg/kg bwt SS, while group VI was exposed to 0.25 mg/kg bwt SS only orally. Following 5 weeks of exposure, levels of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) were increased in SA-exposed groups. Synergistic and antagonistic effects were observed in co-exposed groups depending on dose and the specific tissue being considered. Synergism was observed in tissues co-exposed to higher dose (40 ppm) of SA + 0.25 mg/kgbwt SS except in the liver, where these markers were decreased compared with control. Level of IL-10 (anti-inflammatory marker) decreased in all the tissues investigated except in the lungs of animals co-exposed with 40 ppm SA. There was alteration in tissue architecture, revealing steatosis and hemorrhagic lesions as the common features in co-exposed groups. Results obtained indicate that the dose of SS used in this study may be toxic and not therapeutic against SA-induced tissue inflammation in rats.

Ethylene glycol monomethyl ether (EGME) has been used in many products usually handled by humans including inks, paints, polishes, brake fluids and so on. This present study therefore, investigated its effect on lung, in a time-course study in male Wistar rats. Animals were orally administered 50 mg/kg body weight of EGME for a period of 7, 14, and 21 days. Following 7 days of oral exposure to EGME, activities of GPx and SOD were significantly increased, as well as levels of K-Ras, c-Myc, p53, caspase-3, TNF-α and, IL-6, while NO level and GST activity were significantly reduced compared with control. At the end of 14 days exposure, GSH level was significantly decreased, while levels of K-Ras, c-Myc, p53, caspase-3, TNF-α, IL-6, NO and the activities of SOD and GPx were significantly elevated with respect to control. After 21 days of EGME administration, levels of Bcl-2, IL-10, GSH and NO as well as GST activity were significantly decreased, while levels of K-Ras, c-Myc, p53, Bax, caspase-3, IL-6, IL-1β, TNF-α, as well as GPx, CAT, and SOD activities were significantly elevated compared with control. Lung histopathology revealed chronic disseminated alveolar inflammation, bronchiolitis, severe alveolar and bronchi hyperplasia, severe disseminated inflammation, thrombosis, and thickened vessels as a result of EGME exposures. Exposures to EGME could trigger lung damage via the disorganization of the antioxidant system, eliciting the up-regulation of inflammatory, apoptotic, and oncogenic markers in rats.

2-methoxyethanol (2-ME) is an organic solvent widely used in the manufacture of brake fluids, paints, resins, varnish, nail polish, acetate cellulose, wood coloring, and as a plasticizer in plastics manufacturing. We therefore, investigated its effect on the liver, in a time-course study in male Wistar rats. Animals were orally administered 50 mg/kg body weight of 2-ME for a period of 7, 14, and 21 days. Following 7 days of administration of 2-ME, there was a significant increase in the level of Bax, c-Myc, K-Ras, TNF-α, IL-1β, IL-6, MDA and GPx activity, while the levels of Bcl-2, NO and GSH were significantly reduced compared with control. At the end of 14 days exposure, Bcl-2, and GSH levels, as well as GST activity, were significantly decreased, while levels of Bax, c-Myc, K-Ras, caspase-3, TNF-α, IL-1β, IL-6, MDA and NO were significantly increased compared with control. After 21 days of 2-ME administration, Bcl-2, IL-10, and GSH levels, as well as SOD and GST activities, were significantly decreased, while levels of Bax, c-Myc, K-Ras, caspase-3, p53, TNF-α, IL-1β, IL-6, MDA and NO were significantly increased compared with control. Lastly, liver histopathology confirmed and corroborated the biochemical findings reported above. We therefore, advised that exposures to 2-ME should be strictly avoided as it could trigger hepatic damage through the disorganization of the antioxidant system, up-regulation of inflammatory, apoptotic, and oncogenic markers in rats.

Intermittency of electrical power in developing countries, as well as some European countries such as Turkey, can be eluded by taking advantage of solar energy. Correct prediction of solar radiation constitutes a very important step to take advantage of PV solar panels. We propose an experimental study to predict the amount of solar radiation using a classical artificial neural network (ANN) and deep learning methods. PV panel and solar radiation data were collected at Duzce University in Turkey. Moreover, we included meteorological data collected from the Meteorological Ministry of Turkey in Duzce. Data were collected on a daily basis with a 5-min interval. Data were cleaned and preprocessed to train long-short-term memory (LSTM) and ANN models to predict the solar radiation amount of one day ahead. Models were evaluated using coefficient of determination (R2), mean square error (MSE), root mean squared error (RMSE), mean absolute error (MAE), and mean biased error (MBE). LSTM outperformed ANN with R2, MSE, RMSE, MAE, and MBE of 0.93, 0.008, 0.089, 0.17, and 0.09, respectively. Moreover, we compared our results with two similar studies in the literature. The proposed study paves the way for utilizing renewable energy by leveraging the usage of PV panels.

Ethylene glycol monomethyl ether (EGME) is a major component of paints, lacquers, inks, and automobile brake fluids. As a result, exposures to humans are inevitable. We therefore, investigated in this study, its effect on testicular cells in a time-course manner in male Wistar rats. Animals were orally administered 50 mg/kg body weight of EGME for duration of 7, 14, and 21 days. Following 7 days of the administration, levels of NO and GSH were significantly reduced, while levels of c-Myc, K-Ras, caspase-3, IL-6, TNF-α, and IL-1β were significantly increased compared with control. At the end of 14 days exposure, GPx, and SOD activities, as well as IL-10 level were significantly decreased, while levels of c-Myc, K-Ras, p53, Bax, caspase-3, IL-6, TNF-α, IL-1β, and GST activity were significantly elevated compared with control. After 21 days of EGME administration, Bcl-2, IL-10, and NO levels were significantly decreased, while levels of c-Myc, K-Ras, p53, Bax, caspase-3, IL-6, TNF-α, IL-1β, MDA and GST activity were significantly increased compared with control. After 7, 14, and 21 days of EGME administrations, testis histopathology showed severe loss of seminiferous tubules, the seminiferous epithelium revealed very few spermatocytes, spermatids, spermatogonia, spermatozoa, and Sertoli cells, while the interstitial tissue is eroded, with scanty abnormal Leydig cells, compared with the control that appeared normal. We therefore, concluded that EGME-induced testicular toxicity as a result of EGME administration could be via the disorganization of the endogenous antioxidant systems as well as up-regulation of pro-inflammatory, apoptotic and oncogenic mediators in rats.

Edible camphor (EC) infusions are continually used as an aphrodisiac among other roles. In previous studies, EC had been reported to cause convulsion and seizure in rats. There is a dearth of information associating or relating its consumption to brain inflammation. Therefore, we investigated the effect of various doses of EC in an acute study, on hypothalamic and cerebellar levels of some pro-inflammatory cytokines and chemokines in male Wistar rats. Following administration, cerebellar levels of tumor necrosis factor-alpha (TNF-α), interleukin 1 beta (IL-1β), and interleukin 6 (IL-6) were significantly increased by 2000 and 4000 mg/kg EC, while hypothalamic TNF-α and IL-1β levels were significantly elevated by all the tested doses, and IL-6 level by only 2000 and 4000 mg/kg when compared with control. Besides, EC administration resulted in a significant increase in the expressions of cerebellar and hypothalamic nuclear factor kappa B (NF-kB), cyclooxygenase 2 (COX-2), regulated upon activation normal T cell expressed and secreted (RANTES), and monocyte chemo-attractant protein 1 (MCP-1) in a dose-dependent manner compared with control. Therefore, the misuse and overconsumption of EC could trigger cerebellar and hypothalamic inflammation via EC-induced activation of NF-kB and up-regulation of pro-inflammatory mediators. Keywords: Edible camphor, Cerebellum, Hypothalamus, Pro-inflammation, Cytokines, Chemokines

Background. Liver disease continues to be a major cause of morbidity and mortality in sub-Saharan Africa, including Nigeria, due to the high endemicity of viral hepatitis B. However non-alcoholic fatty liver disease may be an important contributory factor. The impact of fatty liver disease in our region has not been evaluated.AIM. To determine the prevalence of non-alcoholic fatty liver disease (NAFLD) among a population of diabetic (DM) subjects attending the endocrine clinic of LASUTH compared with non-diabetic subjects; ascertain other contributing factors and compare the occurrence of the metabolic syndrome in subjects with and without NAFLD.Methodology. Consecutive patients who satisfy the study criteria were enrolled. An investigator-administered questionnaire was used to determine symptoms of liver disease, followed by physical examination to obtain anthropometric indices as well as signs of liver disease. Abdominal scan was performed to determine radiologic evidence of fatty liver and fasting blood samples were collected from for the measurement of fasting lipid profile, glucose, liver biochemistry and serology for hepatitis B and C markers.Results. One hundred and fifty subjects, mean age 56years (standard deviation = 9, range 20-80 yr) and gender ratio (F: M) of 83:67(55%:45%), were recruited. 106 were diabetics and 44 non-diabetics. The overall prevalence of NAFLD amongst all study subjects was 8.7%. The prevalence rate of NAFLD was higher in the DM cases than in the Control subjects but this difference was not statistically significant (9.5 vs. 4.5%, p = 0.2). Only one of the subjects with fatty liver disease had elevated transaminase levels (steatohepatitis) and also had type 2 DM. Central obesity as measured by waist circumference (WC) and SGPT levels were significantly higher in people with fatty liver. The mean body mass index (BMI) of diabetic and non-diabetic patients was similar (31 vs. 30 kg/m2). The prevalence of the metabolic syndrome was higher in the subjects with NAFLD than in those without fatty liver disease but this difference was not statistically significant (p = 0.8).Conclusion. Non-alcoholic fatty liver disease is present in Africa but is less than what one would expect based on American and European studies.