scholarly journals Cafeteria Diet Feeding in Young Rats Leads to Hepatic Steatosis and Increased Gluconeogenesis under Fatty Acids and Glucagon Influence

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1571 ◽  
Author(s):  
Antonio Maeda Júnior ◽  
Jorgete Constantin ◽  
Karina Utsunomiya ◽  
Eduardo Gilglioni ◽  
Fabiana Gasparin ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Hepatic Steatosis ◽  
Glucose Production ◽  
Cafeteria Diet ◽  
Hepatic Insulin Resistance ◽  
Adult Rats ◽  
Fatty Livers ◽  
14Co2 Production ◽  
Obese Subjects ◽  
Reduced Rate

Gluconeogenesis overstimulation due to hepatic insulin resistance is the best-known mechanism behind elevated glycemia in obese subjects with hepatic steatosis. This suggests that glucose production in fatty livers may differ from that of healthy livers, also in response to other gluconeogenic determinant factors, such as the type of substrate and modulators. Thus, the aim of this study was to investigate the effects of these factors on hepatic gluconeogenesis in cafeteria diet-induced obese adult rats submitted to a cafeteria diet at a young age. The livers of the cafeteria group exhibited higher gluconeogenesis rates when glycerol was the substrate, but lower rates were found when lactate and pyruvate were the substrates. Stearate or glucagon caused higher stimulations in gluconeogenesis in cafeteria group livers, irrespective of the gluconeogenic substrates. An increased mitochondrial NADH/NAD+ ratio and a reduced rate of 14CO2 production from [14C] fatty acids suggested restriction of the citric acid cycle. The higher glycogen and lipid levels were possibly the cause for the reduced cellular and vascular spaces found in cafeteria group livers, likely contributing to oxygen consumption restriction. In conclusion, specific substrates and gluconeogenic modulators contribute to a higher stimulation of gluconeogenesis in livers from the cafeteria group.

Role of free fatty acids in hepatic insulin resistance during late pregnancy in conscious rabbits

1991 ◽  
Vol 260 (6) ◽  
pp. E938-E945 ◽  
Author(s):  
M. Gilbert ◽  
M. C. Pere ◽  
A. Baudelin ◽  
F. C. Battaglia
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Uptake ◽  
Hepatic Insulin Resistance ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Lipid Infusion ◽  
Hepatic Glucose

This study addresses whether elevated free fatty acids (FFA) contribute to the hepatic insulin resistance of pregnancy. We applied a euglycemic hyperinsulinemic clamp with or without Intralipid plus heparin infusion in conscious virgin and pregnant rabbits after an 18-h fast coupled with chronic catheterization of the hepatic and portal veins and femoral artery. A primed constant infusion of [3-3H]glucose was used to determine glucose fluxes. Insulin was infused into a mesenteric vein for 140 min. In pregnant rabbits, basal net hepatic uptake of lactate was almost two times that of nonpregnant rabbits. During a euglycemic hyperinsulinemic clamp there was a decline of approximately 65% in hepatic lactate uptake in nonpregnant rabbits at 80 min, whereas a similar decrease was observed only at 140 min in pregnant rabbits. This effect was blocked by lipid infusion. In the basal state the hepatic uptake of FFA was greater in pregnant than in nonpregnant animals. During the hyperinsulinemic clamp the hepatic uptake dropped by approximately 70 and approximately 30% in nonpregnant and pregnant females, respectively. Lipid infusion did not prevent the hepatic FFA uptake and hepatic ketone body output from decreasing. Hepatic glucose production was totally suppressed in the control period in nonpregnant animals but not during lipid infusion (approximately 65%). Hepatic glucose production was not significantly different between pregnant and nonpregnant rabbits during lipid infusion. Glucose utilization was markedly reduced in nonpregnant animals during lipid infusion to levels comparable with that in pregnant animals.(ABSTRACT TRUNCATED AT 250 WORDS)

FFA cause hepatic insulin resistance by inhibiting insulin suppression of glycogenolysis

2002 ◽  
Vol 283 (1) ◽  
pp. E12-E19 ◽  
Author(s):  
Guenther Boden ◽  
Peter Cheung ◽  
T. Peter Stein ◽  
Karen Kresge ◽  
Maria Mozzoli
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Insulin Infusion ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Hepatic Insulin Resistance ◽  
Elevated Plasma ◽  
Heparin Infusion ◽  
Plasma Ffa ◽  
Endogenous Glucose

Free fatty acids (FFA) have been shown to inhibit insulin suppression of endogenous glucose production (EGP). To determine whether this is the result of stimulation by FFA of gluconeogenesis (GNG) or glycogenolysis (GL) or a combination of both, we have determined rates of GNG and GL (with2H2O) and EGP in 16 healthy nondiabetic volunteers (11 males, 5 females) during euglycemic-hyperinsulinemic (∼450 pM) clamping performed either with or without simultaneous intravenous infusion of lipid plus heparin. During insulin infusion, FFA decreased from 571 to 30 μmol/l ( P < 0.001), EGP from 15.7 to 2.0 μmol · kg−1 · min−1( P < 0.01), GNG from 8.2 to 3.7 μmol · kg−1 · min−1( P < 0.05), and GL from 7.4 to −1.7 μmol · kg−1 · min−1( P < 0.02). During insulin plus lipid/heparin infusion, FFA increased from 499 to 1,247 μmol/l ( P< 0.001). EGP decreased 64% less than during insulin alone (−5.1 ± 0.7 vs. −13.7 ± 3.4 μmol · kg−1 · min−1). The decrease in GNG was not significantly different from the decrease of GNG during insulin alone (−2.6 vs. −4.5 μmol · kg−1 · min−1, not significant). In contrast, GL decreased 66% less than during insulin alone (−3.1 vs. −9.2 μmol · kg−1 · min−1, P < 0.05). We conclude that insulin suppressed EGP by inhibiting GL more than GNG and that elevated plasma FFA levels attenuated the suppression of EGP by interfering with insulin suppression of GL.

1898-P: Colonic Short-Chain Fatty Acids Lower Endogenous Glucose Production

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1898-P
Author(s):  
ADELINA I.L. LANE ◽  
SAVANNA N. WENINGER ◽  
FRANK DUCA
Keyword(s):  
Fatty Acids ◽  
Glucose Production ◽  
Short Chain Fatty Acids ◽  
Endogenous Glucose Production ◽  
Short Chain ◽  
Endogenous Glucose ◽  
Chain Fatty Acids

scholarly journals Feeding diversified protein sources exacerbates hepatic insulin resistance via increased gut microbial branched-chain fatty acids and mTORC1 signaling in obese mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Béatrice S.-Y. Choi ◽  
Noëmie Daniel ◽  
Vanessa P. Houde ◽  
Adia Ouellette ◽  
Bruno Marcotte ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Gut Microbiota ◽  
Protein Source ◽  
Hepatic Insulin Resistance ◽  
Branched Chain Fatty Acids ◽  
Mtorc1 Signaling ◽  
Branched Chain ◽  
Mixed Protein ◽  
Chain Fatty Acids

AbstractAnimal models of human diseases are classically fed purified diets that contain casein as the unique protein source. We show that provision of a mixed protein source mirroring that found in the western diet exacerbates diet-induced obesity and insulin resistance by potentiating hepatic mTORC1/S6K1 signaling as compared to casein alone. These effects involve alterations in gut microbiota as shown by fecal microbiota transplantation studies. The detrimental impact of the mixed protein source is also linked with early changes in microbial production of branched-chain fatty acids (BCFA) and elevated plasma and hepatic acylcarnitines, indicative of aberrant mitochondrial fatty acid oxidation. We further show that the BCFA, isobutyric and isovaleric acid, increase glucose production and activate mTORC1/S6K1 in hepatocytes. Our findings demonstrate that alteration of dietary protein source exerts a rapid and robust impact on gut microbiota and BCFA with significant consequences for the development of obesity and insulin resistance.

scholarly journals Competition of glycerol with other oxidizable substrates in rat brain

1986 ◽  
Vol 237 (1) ◽  
pp. 47-51 ◽  
Author(s):  
M C McKenna ◽  
L I Bezold ◽  
S J Kimatian ◽  
J T Tildon
Keyword(s):  
Rat Brain ◽  
Glutamine Metabolism ◽  
Glycerol Oxidation ◽  
Adult Rats ◽  
Adult Rat ◽  
Rat Pups ◽  
Age Related ◽  
Adult Rat Brain ◽  
14Co2 Production ◽  
Age Related Changes

The rate of conversion of [1,3-14C]glycerol into 14CO2 was measured in the presence and absence of unlabelled alternative substrates in whole homogenates from the brains of young (4-6 and 18-20 days old) and adult rats. Unlabelled glucose decreased 14CO2 production from [1,3-14C]glycerol by about 40% at all ages studied. Unlabelled 3-hydroxybutyrate significantly decreased the 14CO2 production from both low (0.2 mM) and high (2.0 mM) concentrations of glycerol in 4-6- and 18-20-day-old rat pups. However, the addition of 3-hydroxybutyrate had no effect on the rate of 14CO2 production from 2.0 mM-glycerol in adult rats, suggesting that the interaction of 3-hydroxybutyrate with glycerol in adult rat brain is complex and may be related to the biphasic kinetics previously reported for glycerol oxidation. Unlabelled glutamine decreased the production of 14CO2 by brain homogenates from 18-20-day-old and adult rats, but not in 4-6-day-old rat pups. In the converse situation, the addition of unlabelled glycerol to whole brain homogenates had little effect on the rate of 14CO2 production from [6-14C]glucose, 3-hydroxy[3-14C]butyrate and [U-14C]glutamine, although some significant differences were noted. Collectively these results suggest that glycerol and these other substrates may be metabolized in separate subcellular compartments in brain such that the products of glucose, 3-hydroxybutyrate and glutamine metabolism can dilute the oxidation of glycerol, but the converse cannot occur. The data also demonstrate that there are complex age-related changes in the interaction of glycerol with 3-hydroxybutyrate and glutamine. The fact that glycerol oxidation was only partially suppressed by the addition of 1-5 mM-glucose, -3-hydroxybutyrate or -glutamine could also suggest that glycerol may be selectively utilized as an energy substrate in some discrete brain region.

scholarly journals Changes in Adult Rats’ Testis structure Induced by Hypothyroidism and Alleviating Role of L-Carnitine

2019 ◽  
Vol 1 (4) ◽  
pp. 13-28
Author(s):  
Abdelmonem Awad Hegazy ◽  
Manal Mohammad Morsy ◽  
Rania Said Moawad ◽  
Gehad Mohammad Elsayed
Keyword(s):  
Fatty Acids ◽  
Semen Analysis ◽  
Protective Role ◽  
The Body ◽  
Albino Rats ◽  
Adult Rats ◽  
Fatty Acids Metabolism ◽  
Group 3 ◽  
Group 2

Background Hypothyroidism is a metabolic disorder affecting the functions of many tissues in the body including the testis. Testis is rich in the polyunsaturated fatty acids content and lacks strong intrinsic antioxidant system making it prone to such oxidative stress. L-carnitine (LC) regulates long chain fatty acids metabolism; and is considered a valuable antioxidant factor. Aim It was to evaluate the effect of hypothyroidism induced by propylthiouracil (PTU) on rats’ testes and the possible protective role of LC. Methods Forty-eight adult male albino rats were used in this work. The animals were divided into three groups with sixteen animals in each. Group 1 (Control): Animals were kept without medications. Group 2 (PTU-treated): was subjected to administration of PTU; while group 3 (PTU and LC) received both PTU and LC. By the end of the experiment “30 days”, blood samples were taken for hormonal assay; then animals were anaesthetized and sacrificed. Specimens were homogenized for biochemical analysis; epididymal content of each rat was obtained immediately for semen analysis. Testes’ specimens were harvested, prepared and examined by light microscope examination. Results Induced hypothyroidism was noticed to cause histopathological, morphometric and biochemical changes in rat’s testes. LC protected the testicular specimens against such changes; it also improved the seminal quality and quantity as well as testicular structure and biochemistry. Conclusion Hypothyroidism could result in hazards to the structure of testis. Fortunately co-administration of LC might reduce such hazards.

Sign in / Sign up

Export Citation Format

Share Document