Effect of Lupin Flour on Corn Oil–Induced Insulin Resistance in C57BL/6 Mice

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2311-PUB
Author(s):  
ILEANA TERRUZZI ◽  
FERNANDA VACANTE ◽  
PAMELA SENESI ◽  
ANNA MONTESANO ◽  
ROBERTO CODELLA ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Corn Oil

High-fat diet-induced muscle insulin resistance: relationship to visceral fat mass

2000 ◽  
Vol 279 (6) ◽  
pp. R2057-R2065 ◽  
Author(s):  
Jong-Yeon Kim ◽  
Lorraine A. Nolte ◽  
Polly A. Hansen ◽  
Dong-Ho Han ◽  
Kevin Ferguson ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fish Oil ◽  
Fat Mass ◽  
Visceral Fat ◽  
High Fat Diet ◽  
Corn Oil ◽  
High Fat ◽  
Muscle Insulin Resistance ◽  
Visceral Fat Accumulation ◽  
Fat Feeding

It has been variously hypothesized that the insulin resistance induced in rodents by a high-fat diet is due to increased visceral fat accumulation, to an increase in muscle triglyceride (TG) content, or to an effect of diet composition. In this study we used a number of interventions: fish oil, leptin, caloric restriction, and shorter duration of fat feeding, to try to disassociate an increase in visceral fat from muscle insulin resistance. Substituting fish oil (18% of calories) for corn oil in the high-fat diet partially protected against both the increase in visceral fat and muscle insulin resistance without affecting muscle TG content. Injections of leptin during the last 4 days of a 4-wk period on the high-fat diet partially reversed the increase in visceral fat and the muscle insulin resistance, while completely normalizing muscle TG. Restricting intake of the high-fat diet to 75% of ad libitum completely prevented the increase in visceral fat and muscle insulin resistance. Maximally insulin-stimulated glucose transport was negatively correlated with visceral fat mass ( P < 0.001) in both the soleus and epitrochlearis muscles and with muscle TG concentration in the soleus ( P < 0.05) but not in the epitrochlearis. Thus we were unable to dissociate the increase in visceral fat from muscle insulin resistance using a variety of approaches. These results support the hypothesis that an increase in visceral fat is associated with development of muscle insulin resistance.

Insulin resistance induced by high-fructose diet potentiates carbon tetrachloride hepatotoxicity

2010 ◽  
Vol 26 (2) ◽  
pp. 89-104 ◽  
Author(s):  
M. Pooranaperundevi ◽  
MS Sumiyabanu ◽  
P. Viswanathan ◽  
R. Sundarapandiyan ◽  
CV Anuradha
Keyword(s):  
Insulin Resistance ◽  
Carbon Tetrachloride ◽  
Corn Oil ◽  
Control Diet ◽  
Lethal Dose ◽  
Protein Carbonyl ◽  
Contributory Factor ◽  
High Fructose Diet ◽  
High Fructose ◽  
Extent Of Damage

Insulin resistance (IR) is recognized as a contributory factor for a variety of liver diseases. The present study investigates the susceptibility of liver to the toxic actions of carbon tetrachloride (CCl4) in a rat model of IR, induced by feeding a high-fructose diet (60 g/100 g) for 30 days. A sub-lethal dose of CCl4 (2 mL/kg intraperitoneally [i.p.], in corn oil) was administered and the outcome of hepatotoxicity was assessed at 0 hour and at 6, 12, 24 and 36 hours after CCl4 administration. After 30 days of fructose feeding, the rats showed IR, decline in liver antioxidant status and rise in lipid peroxidation. Liver dysfunction in fructose-fed rats was evident from a rise in transaminases, total bilirubin and a decrease in albumin/globulin ratio in plasma and decreases in nitrite, arginase and increase in protein carbonyl and nitrosothiol content in liver. Increased staining for 3-nitro tyrosine (3-NT) antibody was observed in fructose-fed rat liver as compared to control. CCl4 (2 mL/kg) caused 100% mortality in fructose-fed rats within 48 hours, while no death of animals occurred in control. CCl 4 caused liver damage in both control and fructose-fed rats. Time-based studies showed that progressive liver injury occurred only in fructose-fed rats from 0, 6, 12, 24 hours, with a peak at 36 hours. In control diet—fed rats, the extent of damage was maximum at 24 hours, which declined at 36 hours. Thus, the toxic effects of CCl4 are potentiated due to compromised liver function in the setting of IR.

A high-fat diet rich in corn oil reduces spontaneous locomotor activity and induces insulin resistance in mice

2015 ◽  
Vol 26 (4) ◽  
pp. 319-326 ◽  
Author(s):  
Chi Kin Wong ◽  
Amy Botta ◽  
Jason Pither ◽  
Chuanbin Dai ◽  
William T. Gibson ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Locomotor Activity ◽  
High Fat Diet ◽  
Corn Oil ◽  
Spontaneous Locomotor Activity ◽  
High Fat

scholarly journals All-trans-retinoic acid ameliorates atherosclerosis, promotes perivascular adipose tissue browning, and increases adiponectin production in Apo-E mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Małgorzata Kalisz ◽  
Magdalena Chmielowska ◽  
Lidia Martyńska ◽  
Anita Domańska ◽  
Wojciech Bik ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Retinoic Acid ◽  
Corn Oil ◽  
Necrosis Factor Alpha ◽  
Perivascular Adipose Tissue ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Apo E ◽  
And Control

AbstractAll-trans-retinoic acid (atRA), an active metabolite of vitamin A, exerts a potential role in the prevention of cardiovascular diseases. It has been shown that atRA ameliorates atherosclerosis while the exact mechanism underlying this protection remains unknown. This study investigated the influence of atRA on insulin resistance (IR), atherosclerosis, and the process of perivascular adipose tissue (PVAT) browning. Moreover, syntheses of adiponectin, adipokine with anti-atherogenic effects, and tumor necrosis factor-alpha (TNF-α), a pro-inflammatory cytokine, were determined in PVAT. Apolipoprotein E-deficient mice (Apo-E) and control C57BL/6J wild-type mice were treated with atRA (5 mg/kg/day) or vehicle (corn oil) by plastic feeding tubes for 8 weeks. Long-term atRA treatment in Apo-E mice did not affect insulin resistance. AtRa administration ameliorated atherosclerosis, induced PVAT browning, and increased adiponectin production in PVAT in Apo-E mice. Furthermore, atRA increased nitric oxide (NO) level but did not affect adiponectin concentration in the aorta of Apo-E mice. These results indicate that atRA ameliorates atherosclerosis in Apo-E mice. We also observed the browning of PVAT. Besides, atRA increased the synthesis of adiponectin in PVAT and augmented NO level in the aorta in ApoE mice.

Hepatospecific effects of fructose on c-jun NH2-terminal kinase: implications for hepatic insulin resistance

2004 ◽  
Vol 287 (5) ◽  
pp. E926-E933 ◽  
Author(s):  
Yuren Wei ◽  
Michael J. Pagliassotti
Keyword(s):  
Insulin Resistance ◽  
Corn Starch ◽  
Corn Oil ◽  
Control Diet ◽  
Tyrosine Phosphatase ◽  
Glucose Production ◽  
Male Rats ◽  
Hepatic Insulin Resistance ◽  
Time Points ◽  
Protein Levels

Sucrose- and fructose-enriched diets produce hepatic insulin resistance in rats independently of obesity. In humans, fructose infusion results in impaired insulin regulation of glucose production. The aim of the present study was to identify intrahepatic mediators of sucrose- and fructose-induced hepatic insulin resistance. In study 1, male rats were fed a control diet (STD, 68% of energy from corn starch, 12% from corn oil) or a sucrose-enriched diet (HSD, 68% sucrose, 12% corn oil) for 1, 2, or 5 wk. HSD produced hepatic insulin resistance at all time points. Hepatic protein tyrosine phosphatase 1B protein levels and activity were increased at 5 wk only, whereas c-jun NH2-terminal kinase (JNK) activity was increased at all time points. Normalization of JNK activity in hepatocytes isolated from HSD rats improved insulin-stimulated tyrosine phosphorylation of insulin receptor substrate (IRS) proteins and insulin suppression of glucose release. In study 2, male rats were provided STD for 1 wk and then were either fasted or fasted and refed either STD or HSD for 3 or 6 h. Rats refed HSD were characterized by increased hepatic JNK activity and phosphorylation of IRS1 on Ser307 after 6 h only. In study 3, hyperglycemic, hyperinsulinemic pancreatic clamps were performed for 3 or 6 h in the presence or absence of low or high intraportal fructose infusions. High intraportal fructose infusions, which increased portal vein fructose concentration to ∼1 mM, increased hepatic JNK activity and phosphorylation of IRS1 on Ser307 at 6 h only. These data suggest that sucrose- and fructose-induced hepatic insulin resistance are mediated, in part, via activation of JNK activity. Thus high rates of fructose metabolism in the liver appear to acutely activate stress pathways.

Ultrastructural Effects of Acute Kepone Treatment in Rats

1976 ◽  
Vol 34 ◽  
pp. 286-287
Author(s):  
Richard L. Klein ◽  
Åsa K. Thureson-Klein ◽  
Harihara M. Mehendale
Keyword(s):  
Neurological Disorders ◽  
Corn Oil ◽  
Preliminary Investigation ◽  
Reproductive Capacity ◽  
Ultrastructural Changes ◽  
Lipid Deposition ◽  
Severe Toxicity ◽  
Sprague Dawley ◽  
Ether Anesthesia ◽  
Sprague Dawley Rats

KeponeR (decachlorooctahydro-1,3,4-metheno-2H-cyclobuta[cd]pentalen-2-one) is an insecticide effective against ants and roaches. It can cause severe toxicity in fishes, birds, rodents and man. Prominent effects include hepatic lipid deposition and hypertrophy, impairment of reproductive capacity and neurological disorders. Mitochondrial oligomycin-sensitive Mg2+-ATPase is also inhibited. The present study is a preliminary investigation of tissue ultrastructural changes accompanying physiological signs of acute toxicity, which after two days treatment include: pronounced hypersensitivity and tremor, various degrees of anorexia and adipsia, and decreased weight gain.Three different series of adult male Sprague-Dawley rats (Charles River or CD-I) were treated by intubation with Kepone in corn oil at a dose of 50 mg per kg for 3 successive days or at 200 ppm in food for 8 days. After ether anesthesia, rats were immediately perfused via a cannula in the left ventricle with 4% p-formaldehyde and 0.5% glutaraldehyde in Millonig's phosphate buffer at pH 7.2 for 20-30 min at 22°C.

Polychlorinated biphenyl induced hepatocyte alterations

1987 ◽  
Vol 45 ◽  
pp. 716-717
Author(s):  
D.N. Collins ◽  
J.N. Turner ◽  
K.O. Brosch ◽  
R.F. Seegal
Keyword(s):  
Lipid Droplets ◽  
Wistar Rats ◽  
Homovanillic Acid ◽  
Polychlorinated Biphenyl ◽  
Corn Oil ◽  
Environmental Pollutants ◽  
Short Term ◽  
Pcb Congeners ◽  
Urinary Levels ◽  
The Brain

Polychlorinated biphenyls (PCBs) are a ubiquitous class of environmental pollutants with toxic and hepatocellular effects, including accumulation of fat, proliferated smooth endoplasmic recticulum (SER), and concentric membrane arrays (CMAs) (1-3). The CMAs appear to be a membrane storage and degeneration organelle composed of a large number of concentric membrane layers usually surrounding one or more lipid droplets often with internalized membrane fragments (3). The present study documents liver alteration after a short term single dose exposure to PCBs with high chlorine content, and correlates them with reported animal weights and central nervous system (CNS) measures. In the brain PCB congeners were concentrated in particular regions (4) while catecholamine concentrations were decreased (4-6). Urinary levels of homovanillic acid a dopamine metabolite were evaluated (7).Wistar rats were gavaged with corn oil (6 controls), or with a 1:1 mixture of Aroclor 1254 and 1260 in corn oil at 500 or 1000 mg total PCB/kg (6 at each level).

Female sex steroid induced gallbladder epithelium changes and gallstone deposits in female hamsters: TEM and SEM aspects

1993 ◽  
Vol 51 ◽  
pp. 354-355
Author(s):  
S. Karkare ◽  
J. Gilloteaux ◽  
T. R. Kelly
Keyword(s):  
Hormone Receptors ◽  
Corn Oil ◽  
Estrogen Therapy ◽  
Gallstone Formation ◽  
The United States ◽  
Sex Steroid ◽  
Estradiol Valerate ◽  
Surface Epithelium ◽  
Female Sex ◽  
Purina Chow

Approximately 1 million people in the United States alone develop gallstones each year. The incidence is higher in women than in men and the ratio being 4 ≥ 1. A correlation has also been suggested between oral contraceptives and cholelithiasis. In addition, postmenopausal or cancer estrogen therapy has been reported to be a factor responsible for gallstone formation. Female sex hormone receptors have been detected not only in the gallbladder musculature, but also in its epithelium. As a follow up to experiments effectuated in the male and the ovariectomized Syrian hamster, this report shows that, a combination of a low cholesterol diet with female sex steroid treatment contributes to the formation of gallstone-like deposits, while modifying the surface epithelium morphology. Syrian hamsters (F1B strain, BioBreeders, Watertown MA) were housed under 12h light: 12 h dark cycle, at 20 °C, fed Purina chow and water ad libitum. Several duration/treatment groups were studied, but this report will focus on data obtained with the group injected weekly with estradiol valerate (E weekly, s.c. 8-10 μg/100 g.b.w., in corn oil) and with i.m. medroxyprogesterone acetate (DepoProvera Upjohn Co., Kalamazoo, MI; 8-10 mg/100 g.b.w.) for a 3-month period. Other parameters (blood and bile) were also studied but not reported here.

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