scholarly journals Calcium supplementation reverts central adiposity, leptin, and insulin resistance in adult offspring programed by neonatal nicotine exposure

2011 ◽  
Vol 210 (3) ◽  
pp. 349-359 ◽  
Author(s):  
J L Nobre ◽  
P C Lisboa ◽  
A P Santos-Silva ◽  
N S Lima ◽  
A C Manhães ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Leptin Receptor ◽  
Calcium Supplementation ◽  
Dietary Calcium ◽  
Standard Diet ◽  
Adult Offspring ◽  
Nicotine Exposure ◽  
Central Adiposity ◽  
Metabolism Regulation ◽  
The Metabolic Syndrome

Obesity is a worldwide epidemic. Calcium influences energy metabolism regulation, causing body weight loss. Because maternal nicotine exposure during lactation programs for obesity, hyperleptinemia, insulin resistance (IR), and hypothyroidism, we decided to evaluate the possible effect of dietary calcium supplementation on these endocrine dysfunctions in this experimental model. Osmotic minipumps containing nicotine solution (N: 6 mg/kg per day for 14 days) or saline (C) were s.c. implanted in lactating rats 2 days after giving birth (P2). At P120, N and C offspring were subdivided into four groups: 1) C – standard diet; 2) C with calcium supplementation (CCa, 10 g calcium carbonate/kg rat chow); 3) N – standard diet; and 4) N with calcium supplementation (NCa). Rats were killed at P180. As expected, N offspring showed higher visceral and total body fat, hyperleptinemia, lower hypothalamus leptin receptor (OB-R) content, hyperinsulinemia, and higher IR index. Also, higher tyrosine hydroxylase (TH) expression (+51%), catecholamine content (+37%), and serum 25-hydroxyvitamin D3(+76%) were observed in N offspring. Dietary calcium supplementation reversed adiposity, hyperleptinemia, OB-R underexpression, IR, TH overexpression, and vitamin D. However, this supplementation did not reverse hypothyroidism. In NCa offspring,Sirt1mRNA was lower in visceral fat (−37%) and higher in liver (+42%). In conclusion, dietary calcium supplementation seems to revert most of the metabolic syndrome parameters observed in adult offspring programed by maternal nicotine exposure during lactation. It is conceivable that the reduction in fat massper se, induced by calcium therapy, is the main mechanism that leads to the increment of insulin action.

scholarly journals Calcium supplementation prevents obesity, hyperleptinaemia and hyperglycaemia in adult rats programmed by early weaning

2011 ◽  
Vol 107 (7) ◽  
pp. 979-988 ◽  
Author(s):  
Jessica Lopes Nobre ◽  
Patricia Cristina Lisboa ◽  
Natália da Silva Lima ◽  
Juliana Gastão Franco ◽  
José Firmino Nogueira Neto ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Calcium Supplementation ◽  
Resistance Index ◽  
Leptin Resistance ◽  
Free Access ◽  
Standard Diet ◽  
Lactation Period ◽  
Early Weaning ◽  
The Metabolic Syndrome ◽  
Tyrosine Kinase 2

It is known that Ca therapy may have anti-obesity effects. Since early weaning leads to obesity, hyperleptinaemia and insulin resistance, we studied the effect of dietary Ca supplementation in a rat model. Lactating rats were separated into two groups: early weaning (EW) – dams were wrapped with a bandage to interrupt lactation in the last 3 d of lactation and control (C) – dams whose pups had free access to milk during the entire lactation period (21 d). At 120 d, EW and C offspring were subdivided into four groups: (1) C, received standard diet; (2) CCa, received Ca supplementation (10 g of calcium carbonate/kg of rat chow); (3) EW, received standard diet; (4) EWCa, received Ca supplementation similar to CCa. The rats were killed at 180 d. The significance level was at P < 0·05. Adult EW offspring displayed hyperphagia (28 %), higher body weight (9 %) and adiposity (77 %), hyperleptinaemia (twofold increase), hypertriacylglycerolaemia (64 %), hyperglycaemia (16 %), higher insulin resistance index (38 %) and higher serum 25-hydroxyvitamin D3 (fourfold increase), but lower adiponectinaemia:adipose tissue ratio (44 %). In addition, they showed Janus tyrosine kinase 2 and phosphorylated signal transducer and activator of transcription 3 underexpression in hypothalamus (36 and 34 %, respectively), suggesting leptin resistance. Supplementation of Ca for 2 months normalised these disorders. The EW group had no change in serum insulin, thyroxine or triiodothyronine, and Ca treatment did not alter these hormones. In conclusion, we reinforced that early weaning leads to late development of some components of the metabolic syndrome and leptin resistance. Dietary Ca supplementation seems to protect against the development of endocrine and metabolic disorders in EW offspring, maybe through vitamin D inhibition.

scholarly journals A COMPENDIOUS REVIEW ON THE METABOLIC SYNDROME; ITS IMPACT ON THE QUALITY OF LIFE

2018 ◽  
Vol 11 ◽  
Author(s):  
Rajalakshimi V ◽  
Vijey Aanandhi M
Keyword(s):  
Quality Of Life ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Sleep Disturbances ◽  
Pharmacological Therapy ◽  
Lifestyle Changes ◽  
Behavioral Strategies ◽  
Central Adiposity ◽  
The Metabolic Syndrome

Background: Metabolic syndrome (MetS), a comprehensive condition is universally described as a group of several causative factors or abnormalities directly linked with insulin resistance that obviously augment the threat mainly for coronary heart disease, diabetes mellitus Type 2, some types of cancers and sleep disturbances, etc. MetS is a contemporary condition that covers a wide-ranging display of disorders with definite metabolic anomalies demonstrating at different times. Consequently, the threat of MetS remains epidemic. This review will potentially study significant factors such as central adiposity, insulin resistance, hypertension, and dyslipidemia; increased inflammation, environmental factors, and genetic predisposition are involved in MetS development. Purpose: This review provides the available facts to validate the relationship between MetS and quality of life. Methods: A thorough exploration in many search engines such as PubMed, Medline, Science direct, EMBASE, and Google scholar was carried out to recognize qualified studies. Results: Almost all studies suggested that MetS is significantly associated with impair quality of life. Lifestyle intervention holds the early preference and such non-pharmacological therapy combines specific suggestion on diet and physical activity with behavioral strategies. For the individuals, where contributing factors are not sufficiently condensed with lifestyle changes, pharmacological treatment should be considered. Conclusion: Therefore, the current study reviews the outline of literature interrelated with the MetS’s characterization, epidemiological existence, pathological process, and management advance for all the risk factors encompassing metabolic disorder.

scholarly journals Loss of ovarian function in the VCD mouse-model of menopause leads to insulin resistance and a rapid progression into the metabolic syndrome

2009 ◽  
Vol 297 (3) ◽  
pp. R587-R592 ◽  
Author(s):  
Melissa J. Romero-Aleshire ◽  
Maggie K. Diamond-Stanic ◽  
Alyssa H. Hasty ◽  
Patricia B. Hoyer ◽  
Heddwen L. Brooks
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Ovarian Function ◽  
Ovarian Failure ◽  
Rapid Progression ◽  
Standard Diet ◽  
Estrogen Replacement ◽  
Vinylcyclohexene Diepoxide ◽  
Insulin Resistant ◽  
The Metabolic Syndrome

Factors comprising the metabolic syndrome occur with increased incidence in postmenopausal women. To investigate the effects of ovarian failure on the progression of the metabolic syndrome, female B6C3F1 mice were treated with 4-vinylcyclohexene diepoxide (VCD) and fed a high-fat (HF) diet for 16 wk. VCD destroys preantral follicles, causing early ovarian failure and is a well-characterized model for the gradual onset of menopause. After 12 wk on a HF diet, VCD-treated mice had developed an impaired glucose tolerance, whereas cycling controls were unaffected [12 wk AUC HF mice 13,455 ± 643 vs. HF/VCD 17,378 ± 1140 mg/dl/min, P < 0.05]. After 16 wk on a HF diet, VCD-treated mice had significantly higher fasting insulin levels (HF 5.4 ± 1.3 vs. HF/VCD 10.1 ± 1.4 ng/ml, P < 0.05) and were significantly more insulin resistant (HOMA-IR) than cycling controls on a HF diet (HF 56.2 ± 16.7 vs. HF/VCD 113.1 ± 19.6 mg/dl·μU/ml, P < 0.05). All mice on a HF diet gained more weight than mice on a standard diet, and weight gain in HF/VCD mice was significantly increased compared with HF cycling controls. Interestingly, even without a HF diet, progression into VCD-induced menopause caused a significant increase in cholesterol and free fatty acids. Furthermore, in mice fed a standard diet (6% fat), insulin resistance developed 4 mo after VCD-induced ovarian failure. Insulin resistance following ovarian failure (menopause) was prevented by estrogen replacement. Studies here demonstrate that ovarian failure (menopause) accelerates progression into the metabolic syndrome and that estrogen replacement prevents the onset of insulin resistance in VCD-treated mice. Thus, the VCD model of menopause provides a physiologically relevant means of studying how sex hormones influence the progression of the metabolic syndrome.

scholarly journals The metabolic syndrome — a neuroendocrine disorder?

2000 ◽  
Vol 83 (S1) ◽  
pp. S49-S57 ◽  
Author(s):  
Per Björntorp ◽  
Roland Rosmond
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Hpa Axis ◽  
Leptin Receptor ◽  
Psychiatric Disease ◽  
Cortisol Secretion ◽  
The Metabolic Syndrome ◽  
Sympathetic Nervous

Central obesity is a powerful predictor for disease. By utilizing salivary cortisol measurements throughout the day, it has now been possible to show on a population basis that perceived stress-related cortisol secretion frequently is elevated in this condition. This is followed by insulin resistance, central accumulation of body fat, dyslipidaemia and hypertension (the metabolic syndrome). Socio-economic and psychosocial handicaps are probably central inducers of hyperactivity of the hypothalamic–pituitary adrenal (HPA) axis. Alcohol, smoking and traits of psychiatric disease are also involved. In a minor part of the population a dysregulated, depressed function of the HPA axis is present, associated with low secretion of sex steroid and growth hormones, and increased activity of the sympathetic nervous system. This condition is followed by consistent abnormalities indicating the metabolic syndrome. Such ‘burned-out’ function of the HPA axis has previously been seen in subjects exposed to environmental stress of long duration. The feedback control of the HPA axis by central glucocorticoid receptors (GR) seems inefficient, associated with a polymorphism in the 5′ end of the GR gene locus. Homozygotes constitute about 14 % of Swedish men (women to be examined). Such men have a poorly controlled cortisol secretion, abdominal obesity, insulin resistance and hypertension. Furthermore, polymorphisms have been identified in the regulatory domain of the GR gene that are associated with elevated cortisol secretion; polymorphisms in dopamine and leptin receptor genes are associated with sympathetic nervous system activity, with elevated and low blood pressure, respectively. These results suggest a complex neuroendocrine background to the metabolic syndrome, where the kinetics of the regulation of the HPA axis play a central role.

scholarly journals Pengaruh yogurt sinbiotik pisang terhadap kadar glukosa dan insulin tikus sindrom metabolik

2017 ◽  
Vol 14 (1) ◽  
pp. 10 ◽  
Author(s):  
Fiqhi Cahyaningrum Rahmawati ◽  
Kis Djamiatun ◽  
Nyoman Suci
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Blood Glucose ◽  
Treatment Group ◽  
Standard Diet ◽  
Insulin Levels ◽  
Glucose Levels ◽  
The Metabolic Syndrome ◽  
Blood Glucose Levels ◽  
Reduce Blood Glucose

Background: The metabolic syndrome often begins with insulin resistance characterized by hyperinsulinemia and hyperglycemia. Synbiotic yoghurt tanduk banana contains probiotic and prebiotic FOS can improve insulin resistance in metabolic syndrome.Objective: To prove the effect of synbiotic yoghurt tanduk banana can reduce blood glucose levels and insulin levels in metabolic syndrome rats.Method: True-experimental study with randomized controlled group pre-post test design in male wistar rats. Eighteen samples were induced to become metabolic syndrome with high fat fructose diet for 2 weeks and they were divided into 3 groups: control (K) was given standard diet, treatment group 1 (P1), and treatment group 2 (P2) were given sinbiotic yoghurt tanduk banana dose of 0.009 ml/g body weight (BW)/day and 0.018 ml/g BW/day for 2 weeks.Results: The paired t-test showed there were differences of blood glucose levels and insulin levels before and after treatment in P2 group. The Kruskal Wallis test showed there were differences of mean blood glucose levels inter group after treatment (p<0.05). The One-way Anova test showed there were differences of mean insulin levels inter group after treatment (p<0.05). Conclusion: Synbiotic yoghurt tanduk banana can reduce blood glucose levels and insulin levels in metabolic syndrome rat with effective dose is 0.018 ml/grBW/day.

scholarly journals Potential Role of Novel Myokine in Rats-Induced Metabolic Syndrome

2021 ◽  
Vol 12 (3) ◽  
pp. 3305-3315
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Potential Role ◽  
Serum Levels ◽  
Treated Group ◽  
Control Group ◽  
Standard Diet ◽  
The Metabolic Syndrome ◽  
Obesity And Diabetes ◽  
Increased Risk

One of the main health problems is metabolic syndrome (MetS). Its incidence elevates with age leading to a higher risk of evolving chronic diseases and cancer. Obesity and insulin resistance was considered the most vital components in its pathogenesis for a long time. This study aims to evaluate serum novel adipokine and myokine to establish the irrelation of insulin resistance and their impact on metabolic syndrome. Four groups of rats were included; the control group (C) fed with a standard diet, the second group (CI) fed on a standard diet and injected daily with irisin (100ng/ ml) till the end of the experiment. The third group (MetS group) fed on the HCHF diet for 20 weeks and served as a control group. Rats in the fourth group (MetS+I group) were fed on the HCHF diet until they become obese and diabetic, then injected daily with irisin (100ng/ ml) till the end of the experiment and served as a treated group. Serum levels of obesity and diabetes indices were significantly increased while HDL was significantly decreased in the metabolic syndrome group, but after treatment with irisin, their levels were improved. Both adropin and irisin were significantly decreased, while IL-6 was significantly increased in the same group that was enhanced after irisin treatment. In conclusion, this study demonstrated that lower irisin correlates with the increased risk of increased risk of insulin resistance and MetS. In addition, our results suggested that irisin could have a potential role in glucose metabolism. The relations among increased levels of circulating irisin, insulin resistance, and MetS prevalence may be elucidated with a physiological compensatory contrivance.

scholarly journals Early insulin resistance is associated with alterations in gut permeability and microbial activity in rats fed a moderately westernized diet

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Anne-Marie Davila ◽  
Anne Blais ◽  
Marta Grauso Culetto ◽  
Véronique Mathé ◽  
Annaïg Lan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Microbial Activity ◽  
Barrier Function ◽  
Oral Glucose ◽  
Standard Diet ◽  
Low Grade ◽  
The Metabolic Syndrome ◽  
Gut Barrier Function ◽  
Sequence Of Events ◽  
Westernized Diet

AbstractIn Western societies, unbalanced diets may lead to intestinal allostatic stress, with microbial dysbiosis and alteration of the gut barrier function. These local modifications may induce a low-grade inflammation via endotoxemic process, which contribute to systemic alterations clustering into the metabolic syndrome (MetS) and increasing the risk of cardiovascular diseases and type 2 diabetes. We investigated the sequence of events initiating the MetS in rats challenged with a diet that differed moderately from the dietary guidelines, regarding the proportions and nature of energy, carbohydrates, lipids and fibre.Male Wistar rats (265 g upon arrival) were with either a standard diet (Con, n = 10, 3730 kcalkg, 4.0% lipids, 6.3% sucrose, 58.0% starch, 5.0% fibre) or a westernized induction diet (Ind, n = 10, moderately enriched in energy (4120 kcal/kg), lipid (24.0%), and sugars (15%, half sucrose-half fructose), and low in starch (25.5%) and fibre (1.25%). An oral glucose tolerance test (OGTT) was performed after 3 weeks. Rats were euthanized after a further week for body composition and collection of caecum content and tissue samples. LPS-binding protein (LPS-BP) was assayed in plasma; ileum and colon samples were used for measurement of wall barrier function (using Ussing chambers) and microbial activity was assessed in caecum (enzymes and metabolites).Body weight did not differ between Con and Ind groups at any time, as well as the absolute masses and proportions of visceral adipose tissue and liver. Fasting triglyceride, glucose, insulin and LPS-BP concentrations, HOMA index and glucose AUC during the OGTT were similar in both groups. When compared to the Con group, Ind rats showed significantly higher risk markers, i.e.: (1) Insulin AUC (x2); (2) Hepatic triglyceride content (x2.8); (3) Wall permeability at both the para- and transcellular levels (x2.6 and 4.3, respectively) in the ileum (but not in the colon). In the caecum, H2S absolute and relative amounts were twice higher in the Ind group, in relation with 2–3-fold increases in specific and total activities of microbial cysteine desulfhydrase and proteases.Multiple dietary changes mimicking a moderately westernized diet induced an increased ileal permeability and changes in the caecal microbial activity, without evidence of endotoxemia. These perturbations were associated with detrimental rupture of homeostasis at both the splanchnic (hepatic steatosis) and systemic (insulin resistance) levels. In this realistic model, these alterations preceded the occurrence of clinical markers of the MetS (obesity and elevated plasma concentrations of glucose and triglyceride).

Dietary Calcium Supplementation Suppresses Bone Formation in Magnesium-Deficient Rats

2006 ◽  
Vol 76 (3) ◽  
pp. 111-116 ◽  
Author(s):  
Hiroshi Matsuzaki ◽  
Misao Miwa
Keyword(s):  
Bone Formation ◽  
Calcium Supplementation ◽  
Control Diet ◽  
Formation Rate ◽  
Dietary Calcium ◽  
Mineral Apposition Rate ◽  
Control Group ◽  
Deficient Diet ◽  
Bone Formation Rate ◽  
Male Wistar Rats

The purpose of this study was to clarify the effects of dietary calcium (Ca) supplementation on bone metabolism of magnesium (Mg)-deficient rats. Male Wistar rats were randomized by weight into three groups, and fed a control diet (control group), a Mg-deficient diet (Mg- group) or a Mg-deficient diet having twice the control Ca concentrations (Mg-2Ca group) for 14 days. Trabecular bone volume was significantly lower in the Mg - and Mg-2Ca groups than in the control group. Trabecular number was also significantly lower in the Mg - and Mg-2Ca groups than in the control group. Mineralizing bone surface, mineral apposition rate (MAR), and surface referent bone formation rate (BFR/BS) were significantly lower in the Mg - and Mg-2Ca groups than in the control group. Furthermore, MAR and BFR/BS were significantly lower in the Mg-2Ca group than in the Mg - group. These results suggest that dietary Ca supplementation suppresses bone formation in Mg-deficient rats.

1774-P: Maternal Apical Periodontitis Promotes Insulin Resistance in Adult Offspring

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1774-P
Author(s):  
THAÍS V. TSOSURA ◽  
FERNANDO Y. CHIBA ◽  
MARIA S. MATTERA ◽  
RENATO F. PEREIRA ◽  
CLÉA A. GARBIN ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Apical Periodontitis ◽  
Adult Offspring
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