Lycopene alleviates Western diet-induced elevations in anthropometrical indices of obesity, adipose lipids, and other nutritional parameters.

Objective: Given the unrelenting surge in the prevalence of obesity and the intensified efforts aimed at elucidating underlying mechanisms and proffering effective treatments, this study investigated the effects of lycopene on various anthropometrical indices of obesity. Methods: Thirty female Wistar rats were equally divided into two groups and fed either control diet or Western diet. After eight weeks, obese rats (fed Western diet) were divided into three groups (n=5); obese control received the vehicle, while the other two received lycopene (0.2 and 0.4 mg/kg body weight, respectively). Normal rats were grouped into three (n=5) and treated similarly. This treatment lasted for another two weeks, in addition to their respective diets. Afterwards, anthropometrical indices were taken. Results: The weight gain, adiposity index, abdominal and thoracic circumference, body mass index, and Lee index were significantly increased (p<0.05) in the obese rats compared to the normal control, by 108.3%, 102.1%, 81.5%, 97.6%, 47.4%, and 13.9%, respectively. The obese rats had significantly (p<0.05) higher adipose tissue lipid contents, daily feed (37.4%) and energy intake (66.0%), daily weight gain (108.3%), and feed efficiency (25.5%) compared to control. However, the treatment of obese rats with lycopene occasioned a dose-dependent reduction in the elevated anthropometrical and nutritional parameters. In addition, lycopene elicited significant reductions (p<0.05), ranging from 16-54%, in the adipose lipid contents. Conclusion: The data presented here illustrate the positive effects of lycopene on indices of obesity and other anthropometric parameters in obese female rats.

Morin Augmented Myocardial eNOS/cGMP/PKG Signaling Pathway and Abated Oxidative and Inflammo-apoptotic Responses in Diethyl Phthalate and Bisphenol-S Co-Exposed Male Albino Rats.

Cardiac failure accounts for many deaths worldwide. Increasing experimental evidence suggests that exposure to chemicals such as bisphenol-S (BPS) and diethyl phthalate (DEP) exacerbate cardiac injuries. Morin is a flavonoid with reported cardioprotective activity. This study evaluated the modulation of pathways relevant to cardiac endothelial function in rats exposed to BPS and DEP mixture (Mix). Thirty male albino rats were distributed across five groups (n = 6): control received dimethyl sulfoxide (DMSO) as vehicle, Mix dissolved in DMSO, Mix + morin (25 mg/kg), Mix + morin (50 mg/kg), and morin (50 mg/kg). After 21 days of oral exposure at 1 ml/kg bodyweight of the Mix and treatment with morin, the animals were sacrificed, and their hearts were excised for biochemical, histological, immunohistochemical, and gene expression analyses. Exposure to the Mix caused a significant increase in oxidative stress indices (H2O2, malondialdehyde, DNA fragmentation, and advanced oxidation protein products). Also, arginase, phosphodiesterase 5', and the relative expression of TNF-α, interleukin-1ß, Bax, androgen receptor, and vascular endothelial growth factor were markedly increased. In contrast, nitric oxide, reduced glutathione, interleukin-10 levels, superoxide dismutase, catalase, and glutathione peroxidase activities decreased significantly. Furthermore, p-NF-kB-p65 expression increased markedly in the Mix-exposed group. Morin treatment significantly reversed these perturbations in a dose-dependent manner in most instances. This study concludes that morin might offer a cardioprotective effect by enhancing the cardiac endothelial system and attenuating oxidative stress, inflammation, and apoptosis elicited by BPS and DEP co-exposure in male Wistar rats.

Duration effects of alcohol graded concentrations on the extent of lipid peroxidation, testis morphology and sperm quality assessment in Wistar rats.

Alcohol consumption is known to cause an array of alcohol-induced biochemical changes in a biological system. This study investigated the durations effects of different alcohol concentrations (30%, 40%, and 50%) on malondialdehyde levels, testes histology, and sperm characteristics in matured male Wistar rats. The rats were divided into four groups namely thus; control, 30%, 40% and 50%. Control group was orally administered 0% alcohol while, group 30%, 40% and 50% received orally 30%, 40% and 50% of alcohol concentrations (3.20 g/ Kg body weight) respectively for maximum durations of 28 days. On the day 1, 7, 14, 21, and 28, five rats from each group (control, 30%, 40% and 50% alcohol) were sacrificed, and malondialdehyde levels, testes histology, and sperm characteristics were examined. Graded alcohol concentrations caused different detrimental effects on sperm characteristics and induced pathological lesions in the testes. Significant increases in serum, liver and testes malondialdehyde levels were durations independent but almost entirely concentrations dependent. Ultimately, administration of alcohol graded concentration led to loss of sperm motility and testicular degeneration in concentration and durations dependent manner without a concomitant increase in the malondialdehyde levels.

Morin attenuates neurobehavioural deficits, hippocampal oxidative stress, inflammation, and apoptosis in rats co-exposed to bisphenol S and diethyl phthalate.

Endocrine-disrupting pollutants (EDPs) remain pervasive in the environment. Bisphenol S (BPS) and diethyl phthalates (DEP) are commonly used to replace the more toxic EDPs. However, it is unclear if they induce neurotoxicity, like their predecessors. Morin possesses relevant neuro-pharmacological activities. Hence, we sought to evaluate the protective effects of morin against the neurotoxic effects previously reported for EDPs. Male Wistar rats were exposed to a mixture of BPS and DEP (MBD) and treated with morin for 21 days. Behavioural assessments were conducted, and the hippocampal tissues were processed for analysis. Rats exposed to MBD presented anxiety-like behaviours, impaired cognitive and motor functions compared to the control group. MBD exposure induced hyperactivity of neurosignalling enzymes (AChE, ADA, MAO-A) and depleted hippocampal antioxidants (SOD, CAT, GPx, and GSH). MBD exposure increased calcium levels and inhibited total Ca2+-ATPase activity. Levels of reactive species (NO and H2O2) and oxidative damage markers (MDA and AOPP) were significantly (P < 0.05) elevated compared to control. The hippocampal expressions of IL-1ß, TNFα, BAX, and APAF-1 in the MBD-exposed rats were significantly higher compared to control. Correspondingly, NF-κB and caspase-3 pathways were activated in the hippocampus of MBD-exposed rats, while the expressions of IL-10 and BDNF were repressed. However, co-treatment with morin improved the neurobehavioral outcomes, alleviated the hyperactivity of neurosignalling enzymes, while suppressing hippocampal oxidative stress, inflammation, and apoptosis. Histological and stereological evaluations supported these findings. In conclusion, co-exposure to BPS and DEP elicit similar neurotoxic outcomes as their predecessors, while morin confers marked protection against these outcomes.

Inhibition of fat accumulation, lipid dysmetabolism, cardiac inflammation, and improved nitric oxide signalling mediate the protective effects of lycopene against cardio-metabolic disorder in obese female rats.

Obesity, hallmarked by excessive lipid accumulation and dysregulation, continues to escalate the prevalence of cardiometabolic diseases, and is a foremost cause of deaths globally. Alternative therapeutic agents are urgently needed. This study hypothesized that lycopene could proffer beneficial effects against obesity-induced cardiometabolic changes. Obesity was induced using a Western-style diet. Female albino rats (n = 36) were randomized into 6 groups of 6 rats each: normal control, obese control, obese + lycopene (20 mg/kg body weight [b.wt.]), obese + lycopene (40 mg/kg b.wt.), lycopene (20 mg/kg b.wt.), and lycopene (40 mg/kg b.wt.). The study was 10 weeks. Obese rats had significantly higher (P< .05) body weight and total body fat. Lipids (triacylglycerol, cholesterol [CHOL], and free fatty acids), cardiac injury markers (troponin-T, creatine kinase-myocardial band, and malondialdehyde), and cardiovascular risk markers (low-density lipoprotein-CHOL, atherogenic and coronary risk indices) were significantly (P< .05) elevated in obese rats compared with control groups. However, obesity significantly reduced high-density lipoprotein-CHOL and impaired cardiac nitric oxide signalling. Pro-inflammatory mediators (nuclear factor-κB-p65, interleukin-1ß [IL-1ß], and IL-6) transcripts were increased in the heart of obese rats, whereas cardiac IL-10 expression was repressed. Treatment with lycopene reduced lipid concentrations, normalized lipid and lipoprotein metabolism, augmented nitric oxide concentration and IL-10 messenger RNA transcripts, and attenuated the expression of pro-inflammatory mediators. These findings delineate the role of lycopene in the attenuation of cardiometabolic disorders potentiated by obesity.

Buchholzia coriacea seed (wonderful kolanut) alleviates insulin resistance, steatosis, inflammation and oxidative stress in high fat diet model of fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) is a hepatic condition with multiple pathological features and it currently has no specific treatment or approved drug. Wonderful kolanut widely consumed fresh or cooked has been applied in the treatment of numerous diseases in folk medicine. In this study, we evaluate the therapeutic potentials of hydroethanolic extract of defatted Buccholzia coriacea seeds (HEBCS) in NAFLD model. HEBCS was subjected to liquid chromatography - mass spectrometry, and 30 male BALB/c mice (28 ± 2 g) were allocated to three (3) experimental groups (n = 10/group). Mice in group I were fed chow diet (CD); those in group II, high fat diet (HFD) and group III, HFD and 250 mg/kg HEBCS p.o. daily for six weeks. HEBCS alleviates HFD-induced insulin resistance and high plasma insulin and glucose levels. It further alleviates hepatic steatosis, and alters plasma lipid profile. HEBCS also protected against HFD-induced inflammation, oxidative stress and hepatocellular damage. In conclusion, HEBCS alleviated NAFLD in mice via suppression of insulin resistance, hyperlipidemia, inflammation and oxidative stress. PRACTICAL APPLICATIONS: Bioactive polyphenols and alkaloids were identified in hydroethanolic extract of defatted Buccholzia coriacea seeds (HEBCS). This study projects HEBCS as a potential therapeutic agent in the treatment of NAFLD. NAFLD is a multi-factorial condition and therefore, HEBCS is promising considering its multiple-target actions in the current model of NAFLD. HEBCS alleviates insulin resistance, metabolic dysfunction, steatosis, and inflammation in this model. There is a need to further investigate HEBCS in other models of NAFLD as a lead to future use in clinical studies.

Lycopene suppresses palmitic acid-induced brain oxidative stress, hyperactivity of some neuro-signalling enzymes, and inflammation in female Wistar rat.

Neuroinflammation can be triggered by certain high caloric nutrients such as palmitic acid (PA). The effect of lycopene against PA-induced neuroinflammation in female rats has not been as explored. In the present study, thirty rats (weighing 150-200) g were randomly allotted into six groups (n = 5) comprising normal control, PA control, PA + lycopene (0.24 mg/kg), PA + lycopene (0.48 mg/kg), lycopene (0.24 mg/kg), and lycopene (0.48 mg/kg), respectively. After seven weeks of PA challenge (5 mM) including two weeks of lycopene treatment, the brain was excised for analyses. Palmitic acid overload caused significant (p < 0.05) increases in adenosine deaminase, monoamine oxidase-A, nucleotides tri-phosphatase, 5'-nucleotidase, acetylcholine esterase, and myeloperoxidase activities, and malondialdehyde (MDA) levels which were reduced significantly in the lycopene-treated groups. Conversely, catalase and glutathione peroxidase activities, and reduced glutathione levels concentration decreased by 43%, 34%, and 12%, respectively in the PA control groups compared with the Control. Also, PA triggered a decrease in the brain phospholipids (11.43%) and cholesterol (11.11%), but increased triacylglycerol level (50%). Furthermore, upregulated expressions of Interleukin-1ß, Interleukin-6, and NF-ĸB-p65 in the PA control were attenuated, while decreased Interleukine-10 expression was upregulated due to lycopene treatment. Severe brain vacuolation observed in the histology of the PA control rats was normalized by lycopene. This study concludes that lycopene ameliorated PA-induced neuroinflammation, probably via attenuation of oxidative stress, and downregulation of TLR4/ NF-κB -p65 axis.

Lycopene abrogates obesity-provoked hyperactivity of neurosignalling enzymes, oxidative stress and hypothalamic inflammation in female Wistar rats.

Obesity, a global epidemic, has been strongly associated with impairment of brain function. Lycopene has several therapeutic properties and can cross the blood-brain barrier. However, its effects on obesity-provoked brain dysfunction remain unexplored. This study evaluated the potential remediating effects of lycopene on obesity-induced neurological derangements. Thirty-six female Wistar rats (150-200g) were distributed in six groups (n = 6); normal control, obese control, obese + lycopene (20 mg/kg), obese + lycopene (40 mg/kg), normal + lycopene (20 mg/kg), and normal + lycopene (40 mg/kg). Obesity was induced by feeding rats with the Western diet for eight weeks, while normal rats received the control diet. Afterwards, the brain was excised and processed for biochemical, gene expression analyses, and histological evaluations. Obesity-induced brain dysfunction was hallmarked by reduced brain organosomatic index, accumulation of lipids in the cerebrum, and hyperactivity of neurotransmitters-metabolizing enzymes (AChE, ADA, MAO-A, 5'-nucleotidase, and NTPdase). Also, obese rats had decreased antioxidant capacity, with increased oxidative damage, while the expressions of NF-κß p65 and pro-inflammatory cytokines (IL-1ß and IL-6) were elevated in the hypothalamus. These observations were validated by histomorphological evaluations, which showed vacuolation in the brain of obese rats. Treatment with lycopene significantly (p < 0.05) reduced the elevated lipid contents and activities of neuronal enzymes, alleviated oxidative stress and inflammation, while improving the histology of the brain, in a dose-dependent manner. Thus, lycopene abrogates obesity-provoked brain dysfunction and may present a safe and viable therapeutic option for the management of neurological perturbations associated with obesity.

Propolis ethanol extract abrogates hyperglycemia, lipotoxicity, and lowered hepatic poly (ADP-ribose) polymerase protein level in male albino rats.

BACKGROUND AND AIM: Diabetes is a major cause of death worldwide and currently available allopathic drugs presents adverse side effects, thus, necessitating a continuous screening for natural products. This study therefore investigated the effects of Propolis Ethanol Extract (PEE) on blood sugar, lipid metabolism, and poly-(ADP)-ribose polymerase (PARPs) protein level of diabetic male Wistar rats. METHODOLOGY: Seventy rats weighing between (150-180) g used in this study were randomized into seven (7) groups as follows: group 1 (Normal control given Olive oil), group 2 (Diabetic control given Olive oil), group 3 [Diabetic + PEE (200 mg/kg)], group 4 [Diabetic + (PEE 600 mg/kg)], group 5 [Diabetic + Glibenclamide (10 mg/kg)], group 6 [Normal + PEE (200 mg/kg)], and group 7 [Normal + PEE (600 mg/kg)]. Diabetes was induced by a single intraperitoneal injection of streptozotocin (65 mg/kg in 0.1 M citrate buffer pH 4.5), while the vehicle and PEE were orally administered once daily. Treatment with PEE commenced after the confirmation of diabetes. Five rats from each group were sacrificed after the third and sixth weeks of PEE treatment. RESULTS: Administration of PEE significantly (P < 0.05) lowered the elevated fasting blood sugar, improves body weight, and abated lipotoxicity in the brain, heart, liver and kidney of the treated groups in a dose- and duration-dependent manners. The increased protein level of PARPs and lowered hydroxyl methyl-glutaryl CoA reductase activity were significantly reversed after PEE treatment. CONCLUSIONS: This study concludes that PEE might be a suitable and viable regimen against diabetic complications in rats.

A time course study on dose-response relationship between alcohol exposure and its effects on lipid profile and biomarkers of tissue damage.

This present research investigated variations in lipid profiles and important biomarkers of tissue damage in response to graded concentrations of alcohol administration in male Wistar rats. Group A (control) received distilled water while group B, C and D received 30%, 40% and 50% (v/v) alcohol respectively. Five rats each from groups A-D were sacrificed after day(s) 1, 7, 14, 21 and 28 of administration. A significant increase was observed at day 28 for serum cholesterol by 79% (group B), 78% (group C) and 47% (group D) together with serum phospholipid 58% (group B), 50% (group C) and 92% (group D). Serum triacylglycerol increased by 71% (group B), 43% (group C) and 16% (group D) at day 21, while concentration of serum albumin decreased at day 28 by 40.9% (group B), 50.2% (group C), 53.3% (group D) respectively when compared with control (group A). Serum aminotransferases and alkaline phosphatase specific activities, as well as creatinine and uric acid concentration increased in a concentration-dependent manner, following alcohol administration. Though most of these effects induced by alcohol were time- and concentration-dependent, 40% alcohol appear to be more stable, giving results consistent with alcohol-induced damages, with minimal mortality. This study therefore further validated dyslipidemia and imbalance in clinical biomarkers as hallmarks of tissue damage induced by excessive alcohol consumption with an insight on the time- and concentration-response relationship between alcohol consumption and its toxicity.

Oral administration of marijuana produces alterations in serotonin 5-hydroxytryptamine receptor 3A gene (HTR3A) and electrolyte imbalances in brain of male Wistar rats.

The gene expression of serotonin 5-hydroxytryptamine receptor 3A (receptor 3A:HTR3A) as well as the concentration of electrolytes in male Wistar rats after administration of graded doses of marijuana extract was investigated. Twelve groups (3 control and 9 test groups) of 6 animals each were daily exposed to 12.5, 25 and 50 mg/kg b.w doses of petroleum ether extract of marijuana for 4, 8 and 12 weeks. The expressions of the gene were obtained using reverse transcriptase-polymerase chain reaction (RT-PCR) while electrolytes concentrations were determined. An upregulation of over 90% was observed in the expression of HTR3A after exposure to the highest dose throughout the exposure period. There was significant increase in the plasma potassium concentration at all doses while there was a decrease in the brain only at 50 mg/kg dose throughout the exposure period. Sodium concentration in the brain was not affected by the doses over the period of exposure but plasma concentration decreased significantly. All the doses of marijuana extract significantly increased calcium concentration in the brain after prolonged exposure but the plasma concentration remained unchanged. This suggests that different doses of marijuana extract alter the expression of serotonin receptor and electrolyte concentrations over a period of time with possible neurological consequences.

Chitosan from Crabs (Scylla serrata) Represses Hyperlipidemia-Induced Hepato-Renal Dysfunctions in Rats: Modulation of CD43 and p53 Expression.

Hepato-renal dysfunctions associated with hyperlipidemia necessitates a continuous search for natural remedies. This study thus evaluated the effect of dietary chitosan on diet-induced hyperlipidemia in rats. A total of 30 male Wistar rats (90 ± 10) g were randomly allotted into six (6) groups (n = 5): Normal diet, High-fat diet (HFD), and Normal diet + 5% chitosan. The three other groups received HFD, supplemented with 1%, 3%, and 5% of chitosan. The feeding lasted for 6 weeks, after which the rats were sacrificed. The liver and kidneys were harvested for analyses. Hepatic alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) activity, and renal biomarkers (ALT, AST, urea, and creatinine) were assayed spectrophotometrically. Additionally, expression of hepatic and renal CD43 and p53 was estimated immunohistochemically. The HFD group had elevated bodyweight compared to normal which was reversed in the chitosan-supplemented groups. Hyperlipidemia caused a significant (p < 0.05) decrease in the hepatic (AST, ALT, and ALP) and renal (AST and ALT) activities, while renal urea and creatinine increased. Furthermore, the HFD group showed an elevated level of hepatic and renal CD43 while p53 expression decreased. However, groups supplemented with chitosan showed improved hepatic and renal biomarkers, as well as corrected the aberrations in the expressions of p53 and CD43. Conclusively, dietary chitosan inclusion in the diet (between 3% and 5%) could effectively improve kidney and liver functionality via abatement of inflammatory responses.

Bioaccumulation of heavy metals, lipid profiles, and antioxidant status of snails (Achatina achatina) around cement factory vicinities.

Some snails (Achatina spp) can be used as a biosensor of heavy metal poisoning. This study thus estimated some heavy metal levels, antioxidant markers, and lipid profiles of snails handpicked around cement factory vicinities in Ogun State, Nigeria. Snails and soil samples were collected from Oke, Ewekoro, Papalanto, and Mowodani Imeko-Afon (control site). Lead (Pb), cadmium (Cd), and arsenic (As) levels were estimated in the soil, snail foot, hemolymph, and shell using Atomic Absorption Spectrophotometry. Triacylglycerol (TAG), phospholipids (PHOL), cholesterol (CHOL), malondialdehyde (MDA), and reduced glutathione (GSH) levels, as well as glutathione-S-transferase (GST), lactate dehydrogenase (LDH), and arylesterase (AR) activities in the hemolymph, were estimated spectrophotometrically. The snails collected from the Oke site had the highest foot Pb (274.66 ± 13.50 mg/g tissue), CHOL, TAG, PHOL levels, and GST activity when compared with other sites. Snails collected from Papa had the highest Cd levels (1.79 ± 0.74 mg/kg), As (1206 ± 18.87 mg/g tissue) in the foot, and LDH activity, while Ewekoro snails had highest MDA levels and AR activities but the lowest GSH levels. Additionally, there were negative correlations between the heavy metal levels and the activities of GST and AR as well as GSH levels, while positively correlating with LDH activity and MDA level. Workers and the general public around cement factories are at a greater risk of heavy metal-induced pathologies. More so, consumption of snails around these sites may be deleterious to health.

Probiotics consortium synergistically ameliorates aflatoxin B1-induced disruptions in lipid metabolism of female albino rats.

To investigate the effects of oral administration of probiotics consortium on lipid metabolism in aflatoxin B1 (AFB1) exposed rats, ninety female albino rats were first grouped into two: NC (control fed standard feed) and AF (fed AFB1-contaminated feed at 40 ppb). After eight weeks, baseline animals were sacrificed from both groups while the others further divided into four groups - NC treated with and without the probiotics consortium, aflatoxin treated with and without the probiotics consortium (NCT, NCC, AFT, and AFC respectively). Five animals from each group were sacrificed weekly for four weeks, with the collection of blood, liver, brain, and the small intestine. Administration of probiotics instigated significant (p < 0.05) reductions in the elevated plasma and organ lipids as well as HDL-TAG and VLDL + LDL CHO concentrations of animals exposed to AF. AF-induced hepatic lipogenesis and up-regulation of 3-hydroxy-3-methylglutaryl-CoA reductase activity were also significantly (p < 0.05) attenuated following treatment with probiotics in a time-dependent manner. Moreover, neither AF nor probiotics had any effect on glycerol-3-phosphate acyltransferase. Lipid peroxidation was significantly (p < 0.05) reduced in probiotics-treated AF groups, compared to the AF-control groups. This study indicates that the probiotic consortium used synergistically ameliorated the AFB1-induced disruptions in lipid metabolism.

An albino mouse model of nonalcoholic fatty liver disease induced using high-fat liquid "Lieber-DeCarli" diet: a preliminary investigation.

BACKGROUND: Experimental diet models have proven to be vital to understanding the pathophysiology and management of nonalcoholic fatty liver disease (NAFLD). Lieber-DeCarli high-fat, liquid diet have been used to produce NAFLD in rat models. There is, however, currently no information on the effects of this diet in the mouse model. METHODS: Ten (n = 10) male albino mice (27.7 ±â€Š2.0 g) were divided into 2 diet groups (n = 5/group). Animals from group 1 were fed with standard chow diet (CD group) and those from group 2 were fed with Lieber-DeCarli high-fat, liquid diet (high-fat diet or HFD group) ad libitum for a period of 4 weeks. RESULTS: Data obtained show insulin resistance in the HFD group with a significant increase in plasma lipid profile. Level of cholesterol and triglycerides in the liver and plasma increased significantly (P < .05) in the HFD group compared with the CD group. Plasma level of tumor necrosis factor alpha increased significantly in the HFD group compared to control. Also, indicators of oxidative stress (malondialdehyde and protein carbonyls) increased significantly coupled with a significant reduction in reduced glutathione (GSH) level and activity of glutathione peroxidase in the liver of mice in the HFD group compared to CD group. Histopathological evaluation of liver sections reveals steatosis with ballooned hepatocytes. CONCLUSIONS: Data from the present study suggest that the Lieber-DeCarli high-fat, liquid diet may be vital in the study of fatty liver disease in albino mouse. This model may also produce the features of NAFLD in a shorter time in albino mice.

Sapium ellipticum (Hochst.) Pax Ethanol Leaf Extract Maintains Lipid Homeostasis in Streptozotocin-Induced Diabetic Rats.

Dyslipidemia is a common metabolic disorder especially in diabetes mellitus (DM). In this study, the ability of Sapium ellipticum (SE) leaf extract to restore lipid homeostasis in streptozotocin-induced diabetes was examined. DM was induced in experimental rats (Wistar strains) using single intraperitoneal dose (55 mg/kg body weight {BW}) of streptozotocin (STZ). Treatment of diabetic rats with SE was oral (p.o), at doses of 400 and 800 mg kg-1 BW, twice daily at 8 h interval for 21 days. Lipid parameters were analyzed in the serum of rats using test kits. SE caused a significant (P ≤ 0.05) reduction in STZ-induced hypercholesterolemia in a dose dependent pattern (13.7 and 17.89%). These effects were comparable to that provided by metformin (15.45%), a standard antidiabetic drug. Similar pattern was noted with serum triglycerides (TG) (10.63 and 19.06%) and LDL (31.47 and 25.97%). Adipose tissue TG level was improved to near normal. Besides, the cardiovascular risk predictors in terms of atherogenic index of plasma (AIP) and LDL/HDL ratio were lowered by 57.85 and 44.12%, respectively. However, the extract failed to significantly reverse the STZ-induced decline in serum HDL. Overall, with AIP value of 0.28 and LDL/HDL ratio of 0.91, SE demonstrated the potential to maintain lipid homeostasis in the diabetics.

Plasma lipid profiles and risk of cardiovascular disease in occupational lead exposure in Abeokuta, Nigeria.

In order to investigate the effects of lead exposure on risk of cardiovascular disease during occupational exposure to this metal, plasma cholesterol and its fractions as high-density liporotein (HDL), low-density liporotein (LDL) and triglyceride were determined in various artisans in Abeokuta, Nigeria who have been shown to be occupationally exposed to lead and these were related to blood lead levels. Increased risk of cardiovascular disease was observed in the artisans. Total cholesterol in the artisans was between 1.5 and 2.0 times higher in the artisans than that present in controls while LDL cholesterol was between 1.6 and 2.4 times higher in the artisans when compared with control subjects [p < 0.001]. HDL cholesterol and triglyceride levels were not affected [p > 0.05]. A significant positive correlation was observed between blood lead and total cholesterol on one hand [r = 0.372; p = 3.0 x 10(-5)] and blood lead and LDL cholesterol on the other hand [r = 0.283; p = 0.001]. LDL/HDL cholesterol ratio was also higher in the artisans when compared with control. Blood pressure (systolic and diastolic) and other anthropometric parameters were not significantly different between the artisans and the control subjects [p > 0.05]. Results suggest that lead exposure increases cholesterol synthesis and transport to peripheral tissues whereas reverse cholesterol transport to the liver is not affected.