scholarly journals Diet composition and insulin action in animal models

2000 ◽  
Vol 83 (S1) ◽  
pp. S85-S90 ◽  
Author(s):  
Len H. Storlien ◽  
J. A. Higgins ◽  
T. C. Thomas ◽  
M. A. Brown ◽  
H. Q. Wang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Animal Models ◽  
Insulin Action ◽  
Dietary Factors ◽  
Dietary Interventions ◽  
Membrane Function ◽  
Insulin Resistant ◽  
Beneficial Effects ◽  
Saturated Fats ◽  
Major Interest

Critical insights into the etiology of insulin resistance have been gained by the use of animal models where insulin action has been modulated by strictly controlled dietary interventions not possible in human studies. Overall, the literature has moved from a focus on macronutrient proportions to understanding the unique effects of individual subtypes of fats, carbohydrates and proteins. Substantial evidence has now accumulated for a major role of dietary fat subtypes in insulin action. Intake of saturated fats is strongly linked to development of obesity and insulin resistance, while that of polyunsaturated fats (PUFAs) is not. This is consistent with observations that saturated fats are poorly oxidized for energy and thus readily stored, are poorly mobilized by lipolytic stimuli, impair membrane function, and increase the expression of genes associated with adipocyte profileration (making their own home). PUFAs have contrasting effects in each instance. It is therefore not surprising that increased PUFA intake in animal models is associated with improved insulin action and reduced adiposity. Less information is available for carbohydrate subtypes. Early work clearly demonstrated that diets high in simple sugars (in particular fructose) led to insulin resistance. However, again attention has rightly shifted to the very interesting issue of subtypes of complex carbohydrates. While no differences in insulin action have yet been shown, differences in substrate flux suggest there could be long-term beneficial effects on the fat balance of diets enhanced in slowly digested/resistant starches. A new area of major interest is in protein subtypes. Recent results have shown that rats fed high-fat diets where the protein component was from casein or soy were insulin-resistant, but when the protein source was from cod they were not. These are exciting times in our growing understanding of dietary factors and insulin action. While it has been clear for some time that ‘oils ain't oils’, the same is now proving true for carbohydrates and proteins.

scholarly journals CD44 contributes to hyaluronan-mediated insulin resistance in skeletal muscle of high-fat-fed C57BL/6 mice

2019 ◽  
Vol 317 (6) ◽  
pp. E973-E983 ◽  
Author(s):  
Annie Hasib ◽  
Chandani K. Hennayake ◽  
Deanna P. Bracy ◽  
Aimée R. Bugler-Lamb ◽  
Louise Lantier ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
High Fat Diet ◽  
Critical Role ◽  
Chow Diet ◽  
Wild Type ◽  
High Fat ◽  
Insulin Resistant ◽  
Beneficial Effects

Extracellular matrix hyaluronan is increased in skeletal muscle of high-fat-fed insulin-resistant mice, and reduction of hyaluronan by PEGPH20 hyaluronidase ameliorates diet-induced insulin resistance (IR). CD44, the main hyaluronan receptor, is positively correlated with type 2 diabetes. This study determines the role of CD44 in skeletal muscle IR. Global CD44-deficient ( cd44−/−) mice and wild-type littermates ( cd44+/+) were fed a chow diet or 60% high-fat diet for 16 wk. High-fat-fed cd44−/− mice were also treated with PEGPH20 to evaluate its CD44-dependent action. Insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp (ICv). High-fat feeding increased muscle CD44 protein expression. In the absence of differences in body weight and composition, despite lower clamp insulin during ICv, the cd44−/− mice had sustained glucose infusion rate (GIR) regardless of diet. High-fat diet-induced muscle IR as evidenced by decreased muscle glucose uptake (Rg) was exhibited in cd44+/+ mice but absent in cd44−/− mice. Moreover, gastrocnemius Rg remained unchanged between genotypes on chow diet but was increased in high-fat-fed cd44−/− compared with cd44+/+ when normalized to clamp insulin concentrations. Ameliorated muscle IR in high-fat-fed cd44−/− mice was associated with increased vascularization. In contrast to previously observed increases in wild-type mice, PEGPH20 treatment in high-fat-fed cd44−/− mice did not change GIR or muscle Rg during ICv, suggesting a CD44-dependent action. In conclusion, genetic CD44 deletion improves muscle IR, and the beneficial effects of PEGPH20 are CD44-dependent. These results suggest a critical role of CD44 in promoting hyaluronan-mediated muscle IR, therefore representing a potential therapeutic target for diabetes.

scholarly journals Prebiotic prevents impaired kidney and renal Oat3 functions in obese rats

2018 ◽  
Vol 237 (1) ◽  
pp. 29-42 ◽  
Author(s):  
Keerati Wanchai ◽  
Sakawdaurn Yasom ◽  
Wannipa Tunapong ◽  
Titikorn Chunchai ◽  
Parameth Thiennimitr ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Renal Function ◽  
High Fat Diet ◽  
Organic Anion ◽  
Normal Diet ◽  
Organic Anion Transporter ◽  
High Fat ◽  
Insulin Resistant ◽  
Beneficial Effects ◽  
Anion Transporter

Obesity is health issue worldwide, which can lead to kidney dysfunction. Prebiotics are non-digestible foods that have beneficial effects on health. This study aimed to investigate the effects of xylooligosaccharide (XOS) on renal function, renal organic anion transporter 3 (Oat3) and the mechanisms involved. High-fat diet was provided for 12 weeks in male Wistar rats. After that, the rats were divided into normal diet (ND); normal diet treated with XOS (NDX); high-fat diet (HF) and high-fat diet treated with XOS (HFX). XOS was given daily at a dose of 1000 mg for 12 weeks. At week 24, HF rats showed a significant increase in obesity and insulin resistance associated with podocyte injury, increased microalbuminuria, decreased creatinine clearance and impaired Oat3 function. These alterations were improved by XOS supplementation. Renal MDA level and the expression of AT1R, NOX4, p67phox, 4-HNE, phosphorylated PKCα and ERK1/2 were significantly decreased after XOS treatment. In addition, Nrf2-Keap1 pathway, SOD2 and GCLC expression as well as renal apoptosis were also significantly reduced by XOS. These data suggest that XOS could indirectly restore renal function and Oat3 function via the reduction of oxidative stress and apoptosis through the modulating of AT1R-PKCα-NOXs activation in obese insulin-resistant rats. These attenuations were instigated by the improvement of obesity, hyperlipidemia and insulin resistance.

Metabolic responses of horses and ponies to high and low glycaemic feeds: implications for laminitis

2013 ◽  
Vol 53 (11) ◽  
pp. 1182 ◽  
Author(s):  
S. R. Bailey ◽  
N. J. Bamford
Keyword(s):  
Insulin Resistance ◽  
Peak Plasma ◽  
Glycaemic Index ◽  
Dietary Factors ◽  
Metabolic Effects ◽  
Painful Condition ◽  
Insulin Resistant ◽  
Breed Type ◽  
Glycaemic Load ◽  
Equine Metabolic Syndrome

Equine laminitis is the painful condition resulting from disruption of the laminar bonds within the foot. Understanding the dietary triggers may facilitate strategies to prevent laminitis in susceptible animals. The purpose of this review is to examine how dietary factors may lead to insulin resistance and/or excessive insulin production from the pancreas, and why certain breeds or types of horses are more predisposed to this form of laminitis than others. Understanding these relationships will be very important when considering appropriate feeds and the dietary countermeasures necessary for preventing this condition. It is important to note the breed type when considering the likely metabolic effects of dietary carbohydrate, because there are major differences between the Thoroughbred/Standardbred type and some other breeds of horses and ponies. Ponies and certain breeds of horses produce excessive amounts of insulin in response to dietary carbohydrates and this may lead to the development of the three main features of the equine metabolic syndrome, namely obesity, insulin resistance and laminitis. Relative glycaemic index or glycaemic load may be useful in predicting peak plasma insulin (with due consideration for breed type), but carbohydrates such as starch and fructans may have particularly marked effects on insulin sensitivity. Although it is normal for ponies and certain horse breeds to be relatively insulin resistant, it may be possible to reduce the likelihood of exacerbating insulin resistance in obese animals with careful dietary modification. This may help to some extent in reducing hyperinsulinaemia and thereby reducing the risk of laminitis.

scholarly journals Phospholipid Derivatives of Cinnamic Acid Restore Insulin Sensitivity in Insulin Resistance in 3T3-L1 Adipocytes

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3619
Author(s):  
Małgorzata Małodobra-Mazur ◽  
Dominika Lewoń ◽  
Aneta Cierzniak ◽  
Marta Okulus ◽  
Anna Gliszczyńska
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Cinnamic Acid ◽  
Insulin Response ◽  
Aromatic Acids ◽  
Insulin Resistant ◽  
Beneficial Effects ◽  
First Choice ◽  
Derivatives Of

Background: Insulin resistance (IR) is a condition in which the physiological amount of insulin is insufficient to evoke a proper response of the cell, that is, glucose utilization. Metformin is the first choice for therapy, thanks to its glycemic efficacy and general tolerability. In addition, various natural compounds from plant extracts, spices, and essential oils have been shown to provide health benefits regarding insulin sensitivity. In the present study, we analyzed the effect of phospholipid derivatives of selected natural aromatic acids on insulin action and their potential use to overcome insulin resistance. Methods: The 3T3-L1 fibroblasts were differentiated into mature adipocytes; next, insulin resistance was induced by palmitic acid (16:0). Cells were further cultured with phenophospholipids at appropriate concentrations. To assess insulin sensitivity, we measured the insulin-stimulated glucose uptake, using a glucose uptake test. Results: We showed that cinnamic acid (CA) and 3-methoxycinnamic acid (3-OMe-CA) restored the proper insulin response. However, 1,2-dicinnamoyl-sn-glycero-3-phosphocholine (1,2-diCA-PC) and 1-cinnamoyl-2-palmitoyl-sn-glycero-3-phosphocholine (1-CA-2-PA-PC) improved insulin sensitivity in insulin-resistant adipocytes even stronger, exhibiting more beneficial effects. Conclusions: The binding of aromatic acids to phosphatidylcholine increases their beneficial effect on insulin sensitivity in adipocytes and expands their potential practical application as nutraceutical health-promoting agents.

Lack of defect in insulin action on hepatic glycogen synthase and phosphorylase in insulin-resistant monkeys

1998 ◽  
Vol 274 (6) ◽  
pp. G1005-G1010
Author(s):  
Heidi K. Ortmeyer ◽  
Noni L. Bodkin
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Rhesus Monkeys ◽  
Insulin Action ◽  
Glycogen Phosphorylase ◽  
Glycogen Synthase ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
Insulin Resistant

It is well known that an alteration in insulin activation of skeletal muscle glycogen synthase is associated with insulin resistance. To determine whether this defect in insulin action is specific to skeletal muscle, or also present in liver, simultaneous biopsies of these tissues were obtained before and during a euglycemic hyperinsulinemic clamp in spontaneously obese insulin-resistant male rhesus monkeys. The activities of glycogen synthase and glycogen phosphorylase and the concentrations of glucose 6-phosphate and glycogen were measured. There were no differences between basal and insulin-stimulated glycogen synthase and glycogen phosphorylase activities or in glucose 6-phosphate and glycogen contents in muscle. Insulin increased the activities of liver glycogen synthase ( P < 0.05) and decreased the activities of liver glycogen phosphorylase ( P ≤ 0.001). Insulin also caused a reduction in liver glucose 6-phosphate ( P = 0.05). We conclude that insulin-resistant monkeys do not have a defect in insulin action on liver glycogen synthase, although a defect in insulin action on muscle glycogen synthase is present. Therefore, tissue-specific alterations in insulin action on glycogen synthase are present in the development of insulin resistance in rhesus monkeys.

scholarly journals Rat amylin-(8—37) enhances insulin action and alters lipid metabolism in normal and insulin-resistant rats

1997 ◽  
Vol 273 (5) ◽  
pp. E859-E867 ◽  
Author(s):  
M. Hettiarachchi ◽  
S. Chalkley ◽  
S. M. Furler ◽  
Y.-S. Choong ◽  
M. Heller ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Insulin Sensitivity ◽  
Insulin Action ◽  
Glycogen Synthesis ◽  
Human Growth ◽  
Whole Body ◽  
Nonesterified Fatty Acids ◽  
Insulin Resistant

To clarify roles of amylin, we investigated metabolic responses to rat amylin-(8—37), a specific amylin antagonist, in normal and insulin-resistant, human growth hormone (hGH)-infused rats. Fasting conscious rats were infused with saline or hGH, each with and without amylin-(8—37) (0.125 μmol/h), over 5.75 h. At 3.75 h, a hyperinsulinemic (100 mU/l) clamp with bolus 2-deoxy-d-[3H]glucose and [14C]glucose was started. hGH infusion led to prompt (2- to 3-fold) basal hyperamylinemia ( P < 0.02) and hyperinsulinemia. Amylin-(8—37) reduced plasma insulin ( P < 0.001) and enhanced several measures of whole body and muscle insulin sensitivity ( P < 0.05) in both saline- and hGH-infused rats. Amylin-(8—37) corrected hGH-induced liver insulin resistance, increased basal plasma triglycerides and lowered plasma nonesterified fatty acids in both groups, and reduced muscle triglyceride and total long-chain acyl-CoA content in saline-treated rats ( P < 0.05). In isolated soleus muscle, amylin-(8—37) blocked amylin-induced inhibition of glycogen synthesis but had no effect in the absence of amylin. Thus 1) hyperamylinemia accompanies insulin resistance induced by hGH infusion; 2) amylin-(8—37) increases whole body and muscle insulin sensitivity and consistently reduces basal insulin levels in normal and hGH-induced insulin-resistant rats; and 3) amylin-(8—37) elicits a significant alteration of in vivo lipid metabolism. These findings support a role of amylin in modulating insulin action and suggest that this could be mediated by effects on lipid metabolism.

scholarly journals A High Protein Diet Is More Effective in Improving Insulin Resistance and Glycemic Variability Compared to a Mediterranean Diet—A Cross-Over Controlled Inpatient Dietary Study

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4380
Author(s):  
Francesca Tettamanzi ◽  
Vincenzo Bagnardi ◽  
Panayiotis Louca ◽  
Ana Nogal ◽  
Gianna Serafina Monti ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Monitoring ◽  
High Protein Diet ◽  
Glycemic Variability ◽  
High Protein ◽  
Morbidly Obese ◽  
Obese Women ◽  
Dietary Interventions ◽  
Microbiome Composition ◽  
Insulin Resistant

The optimal dietary pattern to improve metabolic function remains elusive. In a 21-day randomized controlled inpatient crossover feeding trial of 20 insulin-resistant obese women, we assessed the extent to which two isocaloric dietary interventions—Mediterranean (M) and high protein (HP)—improved metabolic parameters. Obese women were assigned to one of the following dietary sequences: M–HP or HP–M. Cardiometabolic parameters, body weight, glucose monitoring and gut microbiome composition were assessed. Sixteen women completed the study. Compared to the M diet, the HP diet was more effective in (i) reducing insulin resistance (insulin: Beta (95% CI) = −6.98 (−12.30, −1.65) µIU/mL, p = 0.01; HOMA-IR: −1.78 (95% CI: −3.03, −0.52), p = 9 × 10−3); and (ii) improving glycemic variability (−3.13 (−4.60, −1.67) mg/dL, p = 4 × 10−4), a risk factor for T2D development. We then identified a panel of 10 microbial genera predictive of the difference in glycemic variability between the two diets. These include the genera Coprococcus and Lachnoclostridium, previously associated with glucose homeostasis and insulin resistance. Our results suggest that morbidly obese women with insulin resistance can achieve better control of insulin resistance and glycemic variability on a high HP diet compared to an M diet.

Invited Review: Effects of acute exercise and exercise training on insulin resistance

2002 ◽  
Vol 93 (2) ◽  
pp. 788-796 ◽  
Author(s):  
Erik J. Henriksen
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Exercise Training ◽  
Glucose Tolerance ◽  
Glucose Transport ◽  
Acute Exercise ◽  
Insulin Resistant ◽  
Beneficial Effects ◽  
Glucose Transport System

Insulin resistance of skeletal muscle glucose transport is a key defect in the development of impaired glucose tolerance and Type 2 diabetes. It is well established that both an acute bout of exercise and chronic endurance exercise training can have beneficial effects on insulin action in insulin-resistant states. This review summarizes the present state of knowledge regarding these effects in the obese Zucker rat, a widely used rodent model of obesity-associated insulin resistance, and in insulin-resistant humans with impaired glucose tolerance or Type 2 diabetes. A single bout of prolonged aerobic exercise (30–60 min at ∼60–70% of maximal oxygen consumption) can significantly lower plasma glucose levels, owing to normal contraction-induced stimulation of GLUT-4 glucose transporter translocation and glucose transport activity in insulin-resistant skeletal muscle. However, little is currently known about the effects of acute exercise on muscle insulin signaling in the postexercise state in insulin-resistant individuals. A well-established adaptive response to exercise training in conditions of insulin resistance is improved glucose tolerance and enhanced skeletal muscle insulin sensitivity of glucose transport. This training-induced enhancement of insulin action is associated with upregulation of specific components of the glucose transport system in insulin-resistant muscle and includes increased protein expression of GLUT-4 and insulin receptor substrate-1. It is clear that further investigations are needed to further elucidate the specific molecular mechanisms underlying the beneficial effects of acute exercise and exercise training on the glucose transport system in insulin-resistant mammalian skeletal muscle.

scholarly journals Antidiabetic Activities of Muntingia Calabura L. Leaves Water Extract in Type 2 Diabetes Mellitus Animal Models

2018 ◽  
Vol 10 (2) ◽  
pp. 165-70 ◽  
Author(s):  
Widhya Aligita ◽  
Elis Susilawati ◽  
Ika Kurnia Sukmawati ◽  
Lusi Holidayanti ◽  
Jejen Riswanti
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Animal Model ◽  
Blood Glucose ◽  
Animal Models ◽  
Water Extract ◽  
Control Group ◽  
Insulin Deficiency ◽  
Insulin Resistant ◽  
Muntingia Calabura

BACKGROUND: Diabetes Mellitus (DM) is a heterogeneous group of disorders characterized by increasing blood glucose levels caused by insufficiency of insulin hormone production and activities. There are significant increases in DM case every year in Indonesia, as a consequent, alternative and better drug is needed to be developed. One of the plants that were often used as traditional medicine for DM in Indonesia was Muntingia carabula L. (kersen) leaf. The aim of this research was to evaluate the antidiabetes activity of M. carabula leaves.METHODS: This study was conducted in vivo by evaluating the antidiabetic activity of M. carabula leaf water extract on two animal models, those are insulin deficiency and insulin resistant model animal. The insulin deficiency animal model was developed by aloxan administration at dose of 50 mg/Kg body weight (bw) intravenously. While the insulin resistance animal model was developed by lipid emulsion administration at dose of 0.42 mL/20 grams bw orally. Both groups were randomly devided into 6 groups, which are negative control group, positive control group, standard drug group (glybenclamide 0.65 mg/Kg bw or  metformin 135 mg/Kg bw), and extract groups at dose of 100, 200 and 400 mg/Kg bw. Parameters which were evaluated are fasting blood glucose (FBG) levels for insulin deficiency models and values of constant of insulin tolerance (KITT) for insulin resistant models.RESULTS: In insulin deficient model group, administration of glibenclamide lower the FBG by 43%, furthermore, the extract of M. calabura at doses of 100, 200 and 400 mg/Kg bw also lower the FBG by 13%, 22% and 29%, subsequently. In insulin resistant models, metformin increased the value of KITT from less than 0.5 to 2.91, and administration of the extract at doses of 400, 200 and 100 mg/Kg bw also increased the KITT value to 2.31, 1.57, 1.13, respectively.CONCLUSION: The conclusion was M. carabula leaves water extract with dose of 400 mg/Kg bw had the antidiabetic activities with mechanisms to lower blood glucose level, regenerate pancreatic β cells, and increase insulin sensitivity.KEYWORDS: diabetes mellitus, kersen leaves, Muntingia calabura L., insulin deficiency, insulin resistance

Sign in / Sign up

Export Citation Format

Share Document