scholarly journals SUN-663 Dietary Coconut Oil Mitigates Features of Metabolic Syndrome in Obese Females

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Cassandra Skenandore ◽  
Anisah Ali ◽  
Lesly Gil ◽  
Rani Schwartz ◽  
Camille Goblet ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Serum Insulin ◽  
Coconut Oil ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
Cardiometabolic Health ◽  
High Fat ◽  
Intravenous Glucose

Abstract Forty percent of American women are obese and at risk for metabolic syndrome. Coconut oil alters circulating lipid levels and improves glucose homeostasis in lean individuals, yet, whether it can exert these same beneficial effects on cardiometabolic health in obese individuals is unknown. We hypothesized that female pigs fed a high fat diet with 5% coconut oil would have improvements in features of metabolic syndrome (i.e., dyslipidemia) compared to female mini-pigs fed a high fat diet with 5% lard. We fed female pigs 2200 kcal of a control (n=6), 5000 kcal of a lard high fat (WSD; n=5), or 5000 kcal of a coconut oil high fat (COC; n=6) diet for a total of 9 estrous cycles (~ 7.5 months). Fasting blood was collected at the 1st, 7th (C 7), and 9th (C 9) estrous cycle. After C 7, an intravenous glucose tolerance test (IVGTT) was performed. Weights and morphometric measurements were taken weekly. Tissue was collected for histology at C 9. WSD females (15.14 ± 1.85 mg/dL) had a greater increase in fasting glucose as compared to COC (3.51 ± 4.31 mg/dL) and C females (0.45 ± 3.32 mg/dL; p<0.05). COC females tended to be more glucose tolerant (p=0.07) and had lower serum insulin concentrations in response to a glucose bolus (p<0.001) than WSD females. COC (82.6 ± 1.1 kg) and WSD females (85.4 ± 1.0 kg) weighed more (C: 61.9 ± 1.1 kg; p<0.0001) and had larger abdominal circumferences (COC: 122.4 ± 0.8 cm; WSD: 117.4 ± 1.0 cm) than control females (102.6 ± 1.0 cm; p<0.0001). WSD females were the most dyslipidemic, with the greatest increase in triglycerides (C: 0.33 ± 1.5 mg/dL; COC: 7.71 ± 3.0 mg/dL; WSD: 17.25 ± 3.0 mg/dL; p=0.03) and HDL:cholesterol (C: 3.44 ± 0.22; COC: 5.00 ± 0.36; WSD: 6.00 ± 0.42; p=0.05) as compared control and COC females. COC females had increased plasma docosahexaenoic acid (C: -0.128 ± 0.291; COC: 0.262 ± 0.260; WSD: -0.732 ± 0.274; p<0.01) and decreased arachidonic acid (C: 2.418 ± 0.744; COC: -4.561 ± 0.666; WSD: -2.068 ± 0.702; p<0.01). COC females (131.26 ± 10.0 μm) had a decreased average omental adipocyte diameter as compared to WSD females (160.06 ± 10.31 μm; p=0.05). COC females (7.3 ± 0.80 %) had less hepatic lipid accumulation as measured by oil red o stain than WSD females (9.2 ± 1.1 %; p=0.05). These data demonstrate that small amounts of dietary coconut oil, even as a part of a high fat diet, can mitigate features of metabolic syndrome and decrease hepatic and visceral adipose tissue lipid accumulation in obese females.

Insufficient islet compensation to insulin resistance vs. reduced glucose effectiveness in glucose-intolerant mice

2002 ◽  
Vol 283 (4) ◽  
pp. E738-E744 ◽  
Author(s):  
Bo Ahrén ◽  
Giovanni Pacini
Keyword(s):  
Insulin Secretion ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
Control Diet ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
High Fat ◽  
Intravenous Glucose ◽  
Glucose Effectiveness ◽  
Time Points

This study evaluated the relative contribution of insulin-dependent mechanisms vs. mechanisms independent on dynamic insulin for glucose intolerance induced by high-fat diet. C57BL/6J mice underwent a frequently sampled intravenous glucose tolerance test (1 g/kg glucose) at 1 wk and 1, 3, and 10 mo after initiation of a high-fat diet (58% fat; control diet 11% fat) to measure glucose effectiveness (SG) and disposition index (DI), i.e., insulin sensitivity (SI) times early or total insulin secretion. Glucose disappearance (KG) and SI were reduced in high-fat-fed mice at all time points. Total (50 min) insulin secretion was sufficiently increased at all time points to compensate for the reduced SI, as judged by normal DI50 min. In contrast, early (10 min) insulin secretion was not sufficiently increased; DI10 min was reduced after 1, 3, and 10 mo. SG was reduced after 1 wk; the reduction persisted throughout the study period. Thus glucose intolerance induced by high-fat diet is, in early phases, solely explained by reduced glucose effectiveness, whereas insufficient early insulin secretion is of importance after long-term feeding.

scholarly journals High-fat diet causes increased serum insulin and glucose which synergistically lead to renal tubular lipid deposition and extracellular matrix accumulation

2011 ◽  
Vol 107 (1) ◽  
pp. 74-85 ◽  
Author(s):  
Jun Hao ◽  
Shu-xia Liu ◽  
Song Zhao ◽  
Qing-juan Liu ◽  
Wei Liu ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Extracellular Matrix ◽  
Lipid Droplet ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Serum Insulin ◽  
High Fat ◽  
Renal Tubular ◽  
Matrix Accumulation ◽  
Tgf Β1

Renal tubular lipid accumulation is associated with renal injury in the metabolic syndrome, but its mechanisms are not fully elucidated. The purpose of the present study was to investigate the exact mechanism of renal tubular lipid accumulation in the diet-induced metabolic syndrome. The in vivo experiments showed that a high-fat diet induced hyperglycaemia, hyperinsulinaemia and hypertriacylglycerolaemia, subsequent increases in sterol regulatory element binding protein-1 (SREBP-1) and transforming growth factor-β1 (TGF-β1), lipid droplet deposit in renal tubular cells and interstitial extracellular matrix accumulation in Wistar rats. A human renal proximal tubular epithelial cell line (HKC) was used to determine the direct role of insulin, and the results revealed that insulin induced SREBP-1, fatty acid synthase (FASN), TGF-β1 expressions, lipid droplet and extracellular matrix deposits. Knockdown of SREBP-1 by RNA interference technology significantly inhibited FASN, TGF-β1 up-regulation, lipid and extracellular matrix accumulation caused by insulin. In addition, we found that insulin and high glucose could synergistically increase SREBP-1, FASN, TGF-β1 and fibronectin expressions in HKC cells. These results indicate that high-fat diet-induced increased serum insulin and glucose synergistically cause renal tubular lipid deposit and extracellular matrix accumulation via the SREBP-1 pathway.

scholarly journals The Combination of Ephedrae herba and Coicis semen in Gambihwan Attenuates Obesity and Metabolic Syndrome in High-Fat Diet–Induced Obese Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Jun-Woo Jang ◽  
Dong-Woo Lim ◽  
Ji-Ung Chang ◽  
Jai-Eun Kim
Keyword(s):  
Glucose Tolerance ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Serum Insulin ◽  
Obese Mice ◽  
Hepatic Enzyme ◽  
High Fat ◽  
Cytokine Levels ◽  
The Difference ◽  
Commercial Kits

Gambihwan is a herbal prescription used in Korean medicine to treat obesity. The authors evaluated the effects and mechanisms of two types of Gambihwan (GBH1 and 2) administered to high-fat diet– (HFD-) induced obese mice. Four-week-old C57BL/6 mice were fed a HFD for 8 weeks with or without GBH1 or 2 (100-200 mg/kg/day by oral gavage). All mice were subjected to glucose tolerance testing after the 8-week treatment period and then euthanized. Serum insulin, lipids, and inflammatory cytokine levels were analyzed using commercial kits. Hepatic enzyme levels and lipid profiles were also investigated. Liver section slides were stained with Oil Red O (ORO) or hematoxylin and eosin (H&E) to assess lipid accumulation. GBH1 and 2 both significantly decreased body, liver, or adipose tissue weights in HFD-fed mice and significantly improved glucose tolerance (p<0.05 in all groups). Cholesterol levels in both sera and liver homogenates were significantly decreased by GBH1 and 2 (p<0.05 in all groups). In addition, serum inflammatory cytokines (p<0.05 in 200 mg/kg/day groups) and hepatic enzyme levels were significantly diminished by GBH administration at 200mg/kg/day (p<0.05 in all groups). Furthermore, histologic analyses of liver sections revealed GBH suppressed lipid accumulation. Both GBH types suppressed HFD-induced increases in body weight and obesity-related markers in HFD-fed mice despite the difference in constituents between GBH1 and 2. It is strongly assumed that the combination of Ephedrae herba and Coicis semen exerted the antiobesity effect. The results obtained show that the antiobesity effects of GBH warrant further investigation.

Activated TNF-α/RIPK3 signaling is involved in prolonged high fat diet-stimulated hepatic inflammation and lipid accumulation: inhibition by dietary fisetin intervention

2019 ◽  
Vol 10 (3) ◽  
pp. 1302-1316 ◽  
Author(s):  
Minxuan Xu ◽  
Chenxu Ge ◽  
Yuting Qin ◽  
Tingting Gu ◽  
Jinxiao Lv ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Hepatic Inflammation ◽  
High Fat ◽  
Predisposing Factor ◽  
Nonalcoholic Fatty Liver ◽  
Tnf Α

Increasing evidence indicates that high-fat diet (HFD) is a predisposing factor for metabolic syndrome-associated systemic inflammation and nonalcoholic fatty liver disease (NAFLD).

Relationship of insulin sensitivity to aerobic capacity in Standardbred mares and geldings

2005 ◽  
Vol 2 (3) ◽  
pp. 185-193 ◽  
Author(s):  
SE Pratt ◽  
RJ Geor ◽  
LJ McCutcheon
Keyword(s):  
Insulin Sensitivity ◽  
Aerobic Capacity ◽  
Serum Insulin ◽  
Insulin Response ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
Glucose Disposal ◽  
Intravenous Glucose ◽  
Condition Score ◽  
Relationship Of

AbstractThe objective of this study was to determine the relationship between insulin sensitivity and aerobic capacity and serum adipocytokine (leptin, adiponectin) concentrations in 14 mature, unconditioned Standardbred horses (eight mares, six geldings). Each horse underwent a euglycaemic–hyperinsulinaemic clamp (EHC) and a frequently sampled intravenous glucose tolerance test (FSIGT) for assessment of insulin sensitivity. Aerobic capacity was determined by measurement of the peak rate of oxygen uptake (V˙O2peak) during an incremental exercise test (IET). Serum leptin and adiponectin concentrations were measured in baseline samples obtained before tests of insulin sensitivity. Mean body weight, condition score, V˙O2peak and run time during the IET did not differ between the sex groups. However, minimal model analysis of the FSIGT showed that insulin sensitivity (SI, ×10−4 l mU−1 min−1) was higher (P = 0.002) in geldings (4.21±0.78) than in mares (2.43±0.95), while the acute insulin response to glucose (AIRg) and glucose utilization independent of insulin (SG) were significantly higher in mares. Similarly, glucose uptake (M) per unit of serum insulin (I) during the EHC (M/I ratio) tended (P = 0.08) to be higher in geldings than in mares (×10−2 mg kg−1 min−1 per μU ml−1: 2.41±0.64 vs. 1.80±0.51). There was no significant relationship between V˙O2peak and measures of insulin sensitivity. Stepwise multiple linear regression modelling determined that sex (65%) and leptin concentrations (13.7%) accounted for 78.7% of the variance in SI, while 46% of the variance in M/I could be attributed to sex. It was concluded that aerobic capacity is not an important determinant of insulin-mediated glucose disposal in mature, untrained Standardbred horses. Further studies are needed to examine the influence of gender on insulin sensitivity in horses.

scholarly journals Male and Female Animals Respond Differently to High-Fat Diet and Regular Exercise Training in a Mouse Model of Hyperlipidemia

2021 ◽  
Vol 22 (8) ◽  
pp. 4198
Author(s):  
Melinda E. Tóth ◽  
Brigitta Dukay ◽  
Mária Péter ◽  
Gábor Balogh ◽  
Gergő Szűcs ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
The Body ◽  
Treadmill Running ◽  
Cardiometabolic Health ◽  
Regular Exercise ◽  
High Fat ◽  
Brown Adipose

Inappropriate nutrition and a sedentary lifestyle can lead to obesity, one of the most common risk factors for several chronic diseases. Although regular physical exercise is an efficient approach to improve cardiometabolic health, the exact cellular processes are still not fully understood. We aimed to analyze the morphological, gene expression, and lipidomic patterns in the liver and adipose tissues in response to regular exercise. Healthy (wild type on a normal diet) and hyperlipidemic, high-fat diet-fed (HFD-fed) apolipoprotein B-100 (APOB-100)-overexpressing mice were trained by treadmill running for 7 months. The serum concentrations of triglyceride and tumor necrosis factor α (TNFα), as well as the level of lipid accumulation in the liver, were significantly higher in HFD-fed APOB-100 males compared to females. However, regular exercise almost completely abolished lipid accumulation in the liver of hyperlipidemic animals. The expression level of the thermogenesis marker, uncoupling protein-1 (Ucp1), was significantly higher in the subcutaneous white adipose tissue of healthy females, as well as in the brown adipose tissue of HFD-fed APOB-100 females, compared to males. Lipidomic analyses revealed that hyperlipidemia essentially remodeled the lipidome of brown adipose tissue, affecting both the membrane and storage lipid fractions, which was partially restored by exercise in both sexes. Our results revealed more severe metabolic disturbances in HFD-fed APOB-100 males compared to females. However, exercise efficiently reduced the body weight, serum triglyceride levels, expression of pro-inflammatory factors, and hepatic lipid accumulation in our model.

scholarly journals Kun-Dan Decoction Ameliorates Insulin Resistance by Activating AMPK/mTOR-Mediated Autophagy in High-Fat Diet-Fed Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Zuqing Su ◽  
Kexue Zeng ◽  
Bing Feng ◽  
Lipeng Tang ◽  
Chaoyue Sun ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Oleic Acid ◽  
Insulin Sensitivity ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Tolerance Test ◽  
Network Pharmacology ◽  
High Fat ◽  
Interfering Rna

Background: Metabolic syndrome is characterized by central obesity, hyperglycemia and hyperlipidemia. Insulin resistance is the leading risk factor for metabolic syndrome. Kun-Dan decoction (KD), a traditional Chinese medicine, has been applied to treat patients with metabolic syndrome for over ten years. It is increasingly recognized that autophagy deficiency is the key cause of metabolic syndrome. Therefore, we aimed to explore whether KD can activate autophagy to improve metabolic syndrome.Methods: Network pharmacology was used to explore the underlying mechanism of KD in the treatment of metabolic syndrome. The high-fat diet-fed rats and oleic acid-induced LO2 cells were employed in our study. Oral glucose tolerance test and insulin tolerance test, obesity and histological examination, serum cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), homeostasis model assessment of insulin resistance (HOMA-IR) and insulin sensitivity in high-fat diet-fed rats were analyzed. Furthermore, the protein expressions of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK), phospho-AMPK, mammalian target of rapamycin (mTOR), phospho-mTOR, p62, autophagy related protein (Atg) 5, Atg7, Atg12, Atg13, Atg16L1 and microtubule-associated protein 1A/1B-light chain 3 (LC3)-Ⅱ/Ⅰ were examined in rats and LO2 cells. Moreover, autophagy activator rapamycin and inhibitor 3-methyladenine, and small interfering RNA against Atg7 were utilized to verify the role of autophagy in the treatment of metabolic syndrome by KD in oleic acid-induced LO2 cells.Results: Results from network pharmacology indicated that targeted insulin resistance might be the critical mechanism of KD in the treatment of metabolic syndrome. We found that KD significantly suppressed obesity, serum cholesterol, triglyceride and LDL-C levels and increased serum HDL-C level in high-fat diet-fed rats. Furthermore, KD enhanced insulin sensitivity and attenuated HOMA-IR in high-fat diet-fed rats. Western blot showed that KD could enhance autophagy to increase the insulin sensitivity of high-fat diet-fed rats and oleic acid-induced LO2 cells. Furthermore, 3-methyladenine and small interfering RNA against Atg7 could reverse the protective effect of KD on LO2 cells. However, rapamycin could cooperate with KD to enhance autophagic activation to increase insulin sensitivity in LO2 cells.Conclusion: The induction of autophagy may be the major mechanism for KD to improve insulin resistance and metabolic syndrome.

Postprandial modulation of lipoprotein lipase in rats with insulin resistance

1994 ◽  
Vol 267 (4) ◽  
pp. E620-E627 ◽  
Author(s):  
A. Boivin ◽  
I. Montplaisir ◽  
Y. Deshaies
Keyword(s):  
Glucose Metabolism ◽  
Lipoprotein Lipase ◽  
High Fat Diet ◽  
Serum Insulin ◽  
Vastus Lateralis ◽  
High Fat ◽  
Intravenous Glucose ◽  
High Carbohydrate ◽  
Brown Adipose ◽  
Fat Feeding

The purpose of this study was to determine whether the postprandial modulation of lipoprotein lipase (LPL) activity was altered in rats with resistance of glucose metabolism to insulin action induced by a high-fat diet. Relationships between serum insulin and tissue LPL activity were established in rats chronically fed a high-carbohydrate or high-fat diet, and the effects of fasting and intake of meals of habitual and alternate composition were contrasted. The feeding paradigm did not result in the development of obesity. Global resistance of glucose metabolism to insulin brought about by chronic high-fat feeding was confirmed by an intravenous glucose tolerance test. Fasting serum glucose and insulin concentrations were similar in both cohorts, as was LPL activity in retroperitoneal and inguinal white adipose tissues (WAT), the heart, and soleus. A high-carbohydrate meal brought about higher postprandial insulinemia in the cohort chronically fed the high-fat diet. This was associated with larger changes in LPL activity, that is, an increase in inguinal WAT and in brown adipose tissue and a decrease in soleus, red vastus lateralis, and the heart. Thus the established postprandial modulation of LPL, presumably by insulin, was potentiated in the presence of hyperinsulinemia induced by chronic high-fat feeding despite the concomitant impairment of glucose metabolism.

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