Female rats do not develop sucrose-induced insulin resistance

1997 ◽  
Vol 272 (5) ◽  
pp. R1571-R1576 ◽  
Author(s):  
T. J. Horton ◽  
E. C. Gayles ◽  
P. A. Prach ◽  
T. A. Koppenhafer ◽  
M. J. Pagliassotti
Keyword(s):  
Insulin Resistance ◽  
Female Rats ◽  
Male Rats ◽  
Glucose Kinetics ◽  
Insulin Resistant ◽  
Sucrose Feeding ◽  
Female Wistar Rats ◽  
High Sucrose Feeding ◽  
High Starch ◽  
High Sucrose

In male rats, 2 wk of high-sucrose feeding results in insulin resistance and hypertriglyceridemia [Pagliassotti, M.J., P.A. Prach, T.A. Koppenhafer, and D.A. Pan. Am. J. Physiol. 271 (Regulatory Integrative Comp. Physiol. 40): R1319-R1326, 1996]. The present study aimed to determine if female rats also become insulin resistant and hypertriglyceridemic in response to high-sucrose feeding. Female Wistar rats (7 wk old) were fed either a high-sucrose diet (68% energy) (SU) or a high-starch diet (68% energy) (ST) for 3, 5, or 8 wk. In each animal, glucose kinetics were measured using [3-(3)H]glucose under basal and hyperinsulinemic conditions (insulin infusion 4.0 mU.kg-1.min-1). Body weight and basal glucose kinetics were not different between diet groups at 3, 5, or 8 wk. Glucose infusion rate (mg.kg-1.min-1) was not different between groups (3 wk: 17.7 +/- 1.6 ST, 16.6 +/- 0.9 SU; 5 wk: 16.1 +/- 0.9 ST, 15.1 +/- 2.0 SU; 8 wk: 18.3 +/- 1.9 ST, 16.1 +/- 1.5 SU). Clamp rate of glucose appearance (mg.kg-1.min-1) was also not different between diet groups (3 wk: 4.0 +/- 1.6 ST, 3.6 +/- 1.4 SU; 5 wk: 2.6 +/- 1.0 ST, 2.3 +/- 1.14 SU; 8 wk: 5.9 +/- 1.8 ST, 7.7 +/- 1.2 SU). No difference was observed in plasma and tissue triglycerides or tissue glycogen between sucrose- and starch-fed animals. We therefore conclude that female rats, in contrast to males, do not develop sucrose-induced insulin resistance and hypertriglyceridemia.

scholarly journals Grape Seed Procyanidin Extract Improves Insulin Production but Enhances Bax Protein Expression in Cafeteria-Treated Male Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Lídia Cedó ◽  
Anna Castell-Auví ◽  
Victor Pallarès ◽  
Mayte Blay ◽  
Anna Ardévol ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Grape Seed ◽  
Female Rats ◽  
Male Rats ◽  
Insulin Production ◽  
Prediabetic State ◽  
Insulin Synthesis ◽  
Protein Levels ◽  
Bax Protein ◽  
Female Wistar Rats

In a previous study, the administration of a grape seed procyanidin extract (GSPE) in female Wistar rats improved insulin resistance, reduced insulin production, and modulated apoptosis biomarkers in the pancreas. Considering that pharmacokinetic and pharmacodynamic parameters in females are different from these parameters in males, the aim of the present study was to evaluate the effects of GSPE on male Wistar cafeteria-induced obese rats. The results have confirmed that the cafeteria model is a robust model mimicking a prediabetic state, as these rats display insulin resistance, increased insulin synthesis and secretion, and increased apoptosis in the pancreas. In addition, GSPE treatment (25 mg/kg of GSPE for 21 days) in male rats improves insulin resistance and counteracts the cafeteria-induced effects on insulin synthesis. However, the administration of the extract enhances the cafeteria-induced increase in Bax protein levels, suggesting increased apoptosis. This result contradicts previous results from cafeteria-fed female rats, in which GSPE seemed to counteract the increased apoptosis induced by the cafeteria diet.

scholarly journals TRAF3IP2 (TRAF3 Interacting Protein 2) Mediates Obesity-Associated Vascular Insulin Resistance and Dysfunction in Male Mice

Hypertension ◽  
2020 ◽  
Vol 76 (4) ◽  
pp. 1319-1329
Author(s):  
Zachary I. Grunewald ◽  
Francisco I. Ramirez-Perez ◽  
Makenzie L. Woodford ◽  
Mariana Morales-Quinones ◽  
Salvador Mejia ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Endothelial Cells ◽  
Vascular Dysfunction ◽  
Male Mice ◽  
Wild Type ◽  
High Fat ◽  
Interacting Protein ◽  
Sucrose Feeding ◽  
High Sucrose Feeding ◽  
High Sucrose

Insulin resistance in the vasculature is a characteristic feature of obesity and contributes to the pathogenesis of vascular dysfunction and disease. However, the molecular mechanisms underlying obesity-associated vascular insulin resistance and dysfunction remain poorly understood. We hypothesized that TRAF3IP2 (TRAF3 interacting protein 2), a proinflammatory adaptor molecule known to activate pathological stress pathways and implicated in cardiovascular diseases, plays a causal role in obesity-associated vascular insulin resistance and dysfunction. We tested this hypothesis by employing genetic-manipulation in endothelial cells in vitro, in isolated arteries ex vivo, and diet-induced obesity in a mouse model of TRAF3IP2 ablation in vivo. We show that ectopic expression of TRAF3IP2 blunts insulin signaling in endothelial cells and diminishes endothelium-dependent vasorelaxation in isolated aortic rings. Further, 16 weeks of high fat/high sucrose feeding impaired glucose tolerance, aortic insulin-induced vasorelaxation, and hindlimb postocclusive reactive hyperemia, while increasing blood pressure and arterial stiffness in wild-type male mice. Notably, TRAF3IP2 ablation protected mice from such high fat/high sucrose feeding-induced metabolic and vascular defects. Interestingly, wild-type female mice expressed markedly reduced levels of TRAF3IP2 mRNA independent of diet and were protected against high fat/high sucrose diet-induced vascular dysfunction. These data indicate that TRAF3IP2 plays a causal role in vascular insulin resistance and dysfunction. Specifically, the present findings highlight a sexual dimorphic role of TRAF3IP2 in vascular control and identify it as a promising therapeutic target in vasculometabolic derangements associated with obesity, particularly in males.

scholarly journals S-Nitrosoglutathione Reverts Dietary Sucrose-Induced Insulin Resistance

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 870
Author(s):  
Inês Sousa-Lima ◽  
Ana B. Fernandes ◽  
Rita S. Patarrão ◽  
Young-Bum Kim ◽  
M. Paula Macedo
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Standardized Test ◽  
Whole Body ◽  
Dependent Manner ◽  
Akt Phosphorylation ◽  
Insulin Resistant ◽  
Sucrose Feeding ◽  
High Sucrose

The liver is a fundamental organ to ensure whole-body homeostasis, allowing for a proper increase in insulin sensitivity from the fast to the postprandial status. Hepatic regulation of glucose metabolism is crucial and has been shown to be modulated by glutathione (GSH) and nitric oxide (NO). However, knowledge of the metabolic action of GSH and NO in glucose homeostasis remains incomplete. The current study was designed to test the hypothesis that treatment with S-nitrosoglutathione is sufficient to revert insulin resistance induced by a high-sucrose diet. Male Wistar rats were divided in a control or high-sucrose group. Insulin sensitivity was determined: (i) in the fast state; (ii) after a standardized test meal; (iii) after GSH + NO; and after (iv) S-nitrosoglutathione (GSNO) administration. The fasting glucose level was not different between the control and high-sucrose group. In the liver, the high-sucrose model shows increased NO and unchanged GSH levels. In control animals, insulin sensitivity increased after a meal or administration of GSH+NO/GSNO, but this was abrogated by sucrose feeding. GSNO was able to revert insulin resistance induced by sucrose feeding, in a dose-dependent manner, suggesting that they have an insulin-sensitizing effect in vivo. These effects are associated with an increased insulin receptor and Akt phosphorylation in muscle cells. Our findings demonstrate that GSNO promotes insulin sensitivity in a sucrose-induced insulin-resistant animal model and further implicates that this antioxidant molecule may act as a potential pharmacological tool for the treatment of insulin resistance in obesity and type 2 diabetes.

scholarly journals Role of Ventromedial Hypothalamus in Sucrose-Induced Obesity on Metabolic Parameters

2021 ◽  
pp. 097275312110057
Author(s):  
Archana Gaur ◽  
G.K. Pal ◽  
Pravati Pal
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Food Intake ◽  
Ventromedial Hypothalamus ◽  
Female Rats ◽  
Metabolic Parameters ◽  
Male Rats ◽  
Significant Weight Gain ◽  
The Metabolic Syndrome

Background: Obesity is because of excessive fat accumulation that affects health adversely in the form of various diseases such as diabetes, hypertension, cardiovascular diseases, and many other disorders. Our Indian diet is rich in carbohydrates, and hence the sucrose-induced obesity is an apt model to mimic this. Ventromedial hypothalamus (VMH) is linked to the regulation of food intake in animals as well as humans. Purpose: To understand the role of VMHin sucrose-induced obesity on metabolic parameters. Methods: A total of 24 adult rats were made obese by feeding them on a 32% sucrose solution for 10 weeks. The VMH nucleus was ablated in the experimental group and sham lesions were made in the control group. Food intake, body weight, and biochemical parameters were compared before and after the lesion. Results: Male rats had a significant weight gain along with hyperphagia, whereas female rats did not have a significant weight gain inspite of hyperphagia. Insulin resistance and dyslipidemia were seen in both the experimental and control groups. Conclusion: A sucrose diet produces obesity which is similar to the metabolic syndrome with insulin resistance and dyslipidemia, and a VMH lesion further exaggerates it. Males are more prone to this exaggeration.

Hypothalamo-pituitary regulation of the c-myc gene in rat liver

1990 ◽  
Vol 5 (3) ◽  
pp. 267-274 ◽  
Author(s):  
I. Porsch Hällstöm ◽  
J.-Å. Gustafsson ◽  
A. Blanck
Keyword(s):  
Rat Liver ◽  
Female Rats ◽  
Male Rats ◽  
Female Rat ◽  
Continuous Administration ◽  
Gh Secretion ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Female Wistar Rats ◽  
Myc Gene

ABSTRACT Expression of the c-myc gene was studied in the livers of male and female Wistar rats. Furthermore, the effects on hepatic c-myc expression of neonatal and adult castration, with or without testosterone supplementation, as well as of continuous administration of GH to intact males, were analysed. Expression of c-myc was low in 6-day-old animals of both sexes, reached a maximum at 35 days of age and declined to the level of adult animals at 70 days. In prepubertal animals, expression was higher in females, but was higher in males after the onset of puberty, the postpubertal female rat liver exhibiting 50–70% of the expression in males. Treatment of adult male rats with bovine GH in osmotic minipumps for 1 week reduced c-myc expression to the level of female rats. Castration, both neonatally and of adults, also feminized hepatic c-myc expression. Testosterone supplementation of the castrated animals increased the expression towards the level in sham-operated controls. These results indicate that the c-myc gene is regulated by the hypothalamo-pituitary-liver axis via the sex-differentiated pattern of GH secretion, in analogy with other sex-differentiated hepatic functions, such as metabolism of steroids and xenobiotics. Neuroendocrine regulation of a gene such as c-myc, which is involved in the control of cell proliferation and differentiation, represents another aspect of the complex influence of GH on various somatic functions.

Chronic cerebral hypoperfusion in male rats results in sustained HPA activation, and hyperinsulinemia

2021 ◽  
Author(s):  
Theresa A. Lansdell ◽  
Anne M Dorrance
Keyword(s):  
Insulin Resistance ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Male Rats ◽  
Lower Blood Glucose ◽  
Insulin Resistant ◽  
Lower Blood ◽  
Bilateral Carotid ◽  
Glucose Tolerance Tests ◽  
Bilateral Carotid Artery

Vascular contributions to cognitive impairment and dementia (VCID) is a spectrum of cognitive deficits caused by cerebrovascular disease, for which insulin resistance is a major risk factor. A major cause of VCID is chronic cerebral hypoperfusion (CCH). Under stress, sustained hypothalamic-pituitary-adrenal axis (HPA) activation can result in insulin resistance. Little is known about the effects of CCH on the HPA axis. We hypothesized that CCH causes sustained HPA activation and insulin resistance. Male rats were subjected to bilateral carotid artery stenosis (BCAS) for 12 weeks to induce CCH and VCID. BCAS reduced cerebral blood flow and caused memory impairment. Plasma adrenocorticotropic hormone was increased in the BCAS rats (117.2 ± 9.6 vs. 88.29 ± 9.1 pg/mL, BCAS vs. sham, p = 0.0236), as was corticosterone (220 ± 21 vs. 146 ± 18 ng/g feces, BCAS vs. sham, p = 0.0083). BCAS rats were hypoglycemic (68.1 ± 6.1 vs. 76.5± 5.9 mg/dL, BCAS vs. sham, p = 0.0072), with increased fasting insulin (481.6 ± 242.6 vs. 97.94± 40.02 pmol/L, BCAS vs. sham, p = 0.0003) indicating BCAS rats were insulin resistant (HOMA-IR:11.71 ± 6.47 vs. 2.62 ± 0.93; BCAS vs. control, p = 0.0008). Glucose tolerance tests revealed that BCAS rats had lower blood glucose AUCs than controls (250 ± 12 vs. 326 ± 20 mg/dL/h, BCAS vs. sham, p = 0.0075). These studies indicate that CCH causes sustained activation of the HPA and results in insulin resistance, a condition that is expected to worsen VCID.

SERUM LIPIDS DURING SHORT-TERM HIGH GLUCOSE AND HIGH SUCROSE FEEDING IN INFANTS

PEDIATRICS ◽  
1972 ◽  
Vol 50 (1) ◽  
pp. 84-91
Author(s):  
I. Tamir ◽  
D. Epstein ◽  
D. Heldenberg ◽  
O. Levtow ◽  
B. Werbin
Keyword(s):  
High Glucose ◽  
Caloric Intake ◽  
Serum Triglyceride ◽  
Normal Diet ◽  
Total Serum ◽  
Short Term ◽  
Total Caloric Intake ◽  
Sucrose Feeding ◽  
High Sucrose Feeding ◽  
High Sucrose

The effects of short-term high glucose and high sucrose diets on serum lipids were estimated in six healthy infants aged 4 to 11 months. Each carbohydrate-rich diet was given for 5 days and preceded by 3 days of a "normal" diet. During the high CHO feeding, sucrose or glucose supplied 73% of the total caloric intake, while on the "normal" diet only 40% for the total caloric intake was derived from CHO (glucose only). The percentage of total caloric intake supplied by protein was almost identical in the three diets used. An increase in serum triglyceride (TG) concentration, of almost equal magnitude, was seen following both high CHO feeding periods. Upon resumption of the "normal" diet, serum TG concentrations approached initial concentrations. No consistent changes occurred in total serum cholesterol concentrations or in total serum phospholipid concentrations. A significant increase in the percentage concentration of palmitoleic acid of serum triglyceride fatty acids occurred on both high CHO diets. This increase was slightly but not significantly greater following high sucrose feeding. A significant decrease in the percentage concentration of linoleic acid of serum triglyceride fatty acids occurred on both high CHO diets. This decrease was slightly but not significantly greater following high sucrose feeding. Therefore, it seems that on a short-term basis, high sucrose and high glucose feeding, in healthy infants, will result in similar changes in serum triglyceride concentrations and serum triglyceride fatty acid patterns.

Insulin sensitivity, leptin, adiponectin, resistin, and testosterone in adult male and female rats after maternal-neonatal separation and environmental stress

2018 ◽  
Vol 314 (1) ◽  
pp. R12-R21 ◽  
Author(s):  
Hershel Raff ◽  
Brian Hoeynck ◽  
Mack Jablonski ◽  
Cole Leonovicz ◽  
Jonathan M. Phillips ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adult Male ◽  
Rat Model ◽  
Female Rats ◽  
Male Rats ◽  
Male And Female ◽  
Neonatal Hypoxia ◽  
Male And Female Rats ◽  
Plasma Leptin ◽  
Neonatal Separation

Care of premature infants often requires parental and caregiver separation, particularly during hypoxic and hypothermic episodes. We have established a neonatal rat model of human prematurity involving maternal-neonatal separation and hypoxia with spontaneous hypothermia prevented by external heat. Adults previously exposed to these neonatal stressors show a sex difference in the insulin and glucose response to arginine stimulation suggesting a state of insulin resistance. The current study used this cohort of adult rats to evaluate insulin resistance [homeostatic model assessment of insulin resistance (HOMA-IR)], plasma adipokines (reflecting insulin resistance states), and testosterone. The major findings were that daily maternal-neonatal separation led to an increase in body weight and HOMA-IR in adult male and female rats and increased plasma leptin in adult male rats only; neither prior neonatal hypoxia (without or with body temperature control) nor neonatal hypothermia altered subsequent adult HOMA-IR or plasma adiponectin. Adult male-female differences in plasma leptin were lost with prior exposure to neonatal hypoxia or hypothermia; male-female differences in resistin were lost in the adults that were exposed to hypoxia and spontaneous hypothermia as neonates. Exposure of neonates to daily hypoxia without spontaneous hypothermia led to a decrease in plasma testosterone in adult male rats. We conclude that neonatal stressors result in subsequent adult sex-dependent increases in insulin resistance and adipokines and that our rat model of prematurity with hypoxia without hypothermia alters adult testosterone dynamics.

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