scholarly journals A Calcium-Deficient Diet in Dams during Gestation Increases Insulin Resistance in Male Offspring

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1745 ◽  
Author(s):  
Junji Takaya ◽  
Sohsaku Yamanouchi ◽  
Jiro Kino ◽  
Yuko Tanabe ◽  
Kazunari Kaneko
Keyword(s):  
Insulin Resistance ◽  
Serum Insulin ◽  
Control Diet ◽  
Insulin Resistance Syndrome ◽  
Control Group ◽  
Β Cells ◽  
Deficient Diet ◽  
Ca Deficiency ◽  
Female Wistar Rats ◽  
Deficient Group

Calcium (Ca) plays an important role in the pathogenesis of insulin resistance syndrome. Osteocalcin (OC), a bone formation biomarker, acts directly on β-cells and increases insulin secretion. We determined the effects of Ca deficiency during pregnancy and/or lactation on insulin resistance in offspring. Female Wistar rats consumed either a Ca-deficient or control diet ad libitum from three weeks preconception to 21 days postparturition. Pups were allowed to nurse their original mothers until weaning. The offspring were fed a control diet beginning at weaning and were killed on day 180. Serum carboxylated OC (Gla-OC) and undercarboxylated OC (Glu-OC), insulin and adipokines in offspring were measured. In males, mean levels of insulin, glucose, and HOMA-IR were higher in the Ca-deficient group than in the control group. In addition, ionized Ca (iCa) was inversely associated with serum Glu-OC and adiponectin in males. In females, mean levels of Glu-OC and Gla-OC in the Ca-deficient group were higher than in the control group. In all offspring, serum leptin levels were correlated with serum insulin levels, and inversely correlated with iCa. In conclusion, maternal Ca restriction during pregnancy and/or lactation influences postnatal offspring Ca metabolism and insulin resistance in a sex-specific manner.

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.

microRNA-4458 Regulates Insulin Resistance in Hepatic Cells by Targeting the Insulin-Like Growth Factor 1 Receptor

2021 ◽  
Vol 11 (9) ◽  
pp. 1812-1817
Author(s):  
Jingjing Zhou ◽  
Wenjuan Zhu ◽  
Zheng Mao ◽  
Zhen Li ◽  
Xiaoqin Li ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Mrna Expression ◽  
Glucose Uptake ◽  
Hepg2 Cell ◽  
Molecular Mechanisms ◽  
Cell Model ◽  
Serum Insulin ◽  
Luciferase Reporter ◽  
Control Group ◽  
Hepatic Cells

Background: The objective of the research was to investigate the roles of miR-4458 in the regulation of insulin resistance in hepatic cells and to explore the underlying molecular mechanisms. Methods: The blood samples were collected from the T2D patients and the health controls, and the liver tissues were collected from the DM and control rats. The relationship between IGF1R and miR-4458 was predicted by TargetScan and verified by the dual luciferase reporter gene system. qRT-PCR was used to measure the mRNA expression of miR-4458, IGF1R, G6Pase and PEPCK. The protein expression of IGF1R, p-AKT and AKT were measured by Western blot analysis. The rat insulin ELISA Kit and glucose Uptake Colorimteric Assay Kit were used to determine the level of serum insulin and the glucose uptake. Results: miR-4458 was high expressed in T2D patients. We predicted and verified that IGF1R was a direct target of miR-4458, and the mRNA expression of IGF1R was reduced in type 2 diabetes patients. We established the diabetes model (DM) and IR HepG2 cell model, and found that the blood glucose and serum insulin levels were significantly elevated in the DM group. miR-4458 expression was up-regulated, while the expression of IGF1R and p-AKT, and p-AKT/AKT ratio were reduced in the DM group and IR HepG2 cell model. miR-4458 inhibitor and IGF1R-siRNA significantly decreased the expression of miR-4458 and IGF1R respectively. In comparison with IR+inhibitor control group, miR-4458 inhibitor increased 2-DG6P content, IGF1R expression, p-AKT expression and p-AKT/AKT ratio, reduced the expression of G6Pase and PEPCK, and all the effects were reversed by down-regulating IGF1R. Conclusion: miR-4458 regulated the insulin resistance in hepatic cells by regulating the IGF1R/PI3K/AKT signal pathway, which will be a potential target for the treatment of diabetes.

scholarly journals Endothelial dysfunction precedes hypertension in diet-induced insulin resistance

1998 ◽  
Vol 275 (3) ◽  
pp. R788-R792 ◽  
Author(s):  
Prasad V. G. Katakam ◽  
Michael R. Ujhelyi ◽  
Margarethe E. Hoenig ◽  
Allison Winecoff Miller
Keyword(s):  
Insulin Resistance ◽  
Endothelial Dysfunction ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Mesenteric Arteries ◽  
Control Group ◽  
Sprague Dawley ◽  
Insulin Resistant ◽  
Glucose Levels

The insulin-resistant (IR) syndrome may be an impetus for the development of hypertension (HTN). Unfortunately, the mechanism by which this could occur is unclear. Our laboratory and others have described impaired endothelium-mediated relaxation in IR, mildly hypertensive rats. The purpose of the current study is to determine if HTN is most likely a cause or result of impaired endothelial function. Sprague-Dawley rats were randomized to receive a fructose-rich diet for 3, 7, 10, 14, 18, or 28 days or were placed in a control group. The control group received rat chow. After diet treatment, animals were instrumented with arterial cannulas, and while awake and unrestrained, their blood pressure (BP) was measured. Subsequently, endothelium-mediated relaxation to acetylcholine was determined (in vitro) by measuring intraluminal diameter of phenylephrine-preconstricted mesenteric arteries (∼250 μM). Serum insulin levels were significantly elevated in all groups receiving fructose feeding compared with control, whereas there were no differences in serum glucose levels between groups. Impairment of endothelium-mediated relaxation starts by day 14 [mean percent maximal relaxation (Emax): 69 ± 10% of baseline] and becomes significant by day 18 (Emax: 52 ± 11% of baseline; P < 0.01). However, the mean BP (mmHg) does not become significantly elevated until day 28 [BP: 132 ± 1 ( day 28) vs. 116 ± 3 (control); P < 0.05]. These findings demonstrate that both IR and endothelial dysfunction occur before HTN in this model and suggest that endothelial dysfunction may be a mechanism linking insulin resistance and essential HTN.

scholarly journals Response of diamine oxidase and other plasma copper biomarkers to various dietary copper intakes in the rat and evaluation of copper absorption with a stable isotope

2000 ◽  
Vol 83 (5) ◽  
pp. 561-568 ◽  
Author(s):  
C. Feillet-Coudray ◽  
C. Coudray ◽  
D. Bayle ◽  
E. Rock ◽  
Y. Rayssiguier ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Intestinal Absorption ◽  
Diamine Oxidase ◽  
Control Diet ◽  
The Other ◽  
Control Group ◽  
Deficient Diet ◽  
Apparent Absorption ◽  
Cu Deficiency ◽  
Cu Isotope

There is a lack of agreement on index of Cu status and reliable and sensitive biomarkers are still required. The purpose of this present work was to assess in rats the sensitivity of diamine oxidase (DAO) activity, a recently proposed biomarker, to modifications in dietary Cu intake in comparison with other plasma biomarkers of Cu status. We also evaluated the effect of Cu dietary level on Cu and Zn intestinal absorption. Results showed that plasma Cu and plasma caeruloplasmin were significantly decreased at day 8 compared with the control group (7·4 mg Cu/kg diet) while DAO activity was significantly decreased at day 12 of the deficient diet (0·61 mg Cu/kg diet). Cu supplementation (35 mg Cu/kg diet) had no effect on any of the studied biomarkers of Cu status. In Cu-deficient rats plasma Cu and DAO activities were normalized 4 d after return to the control diet while caeruloplasmin was normalized later, at day 11. Apparent absorption values (%) of total Cu or65Cu isotope were significantly increased in the Cu-deficient rats compared with the other groups and similar in the control and the Cu-supplemented groups. The urinary excretion of total Cu or65Cu isotope were increased in the Cu-supplemented group compared with the other two groups. Both apparent absorption and urinary excretion of total Zn or67Zn isotope remained unchanged in the three experimental groups. In conclusion, DAO activity seemed to be less sensitive to Cu deficiency than plasma Cu or caeruloplasmin concentrations. The present study also showed a significant increase in Cu intestinal absorption with dietary Cu restriction but no decrease with Cu supplementation in the rat.

Comparison of Two Autoimmune Dysglycemia Syndromes: Insulin Autoimmune Syndrome (IAS) and Type B Insulin Resistance Syndrome (B-IRS)

2019 ◽  
Vol 51 (11) ◽  
pp. 723-728 ◽  
Author(s):  
Sui Yu ◽  
Guoqing Yang ◽  
Jingtao Dou ◽  
Baoan Wang ◽  
Weijun Gu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Serum Insulin ◽  
Insulin Resistance Syndrome ◽  
Tolerance Test ◽  
White Blood Count ◽  
Oral Glucose ◽  
Type B ◽  
Insulin Autoimmune Syndrome ◽  
Autoimmune Syndrome ◽  
Clinical Differential Diagnosis

AbstractInsulin autoimmune syndrome (IAS) and type B insulin resistance syndrome (B-IRS) are rare autoimmune dysglycemia syndromes, but their treatment and prognosis are different. This study aimed to provide a basis for the clinical differential diagnosis of IAS and B-IRS. This was a retrospective study of the medical records of all patients diagnosed with IAS or B-IRS between January 2006 and March 2018 at the Chinese PLA General Hospital. Demographic, clinical, biochemistry, treatment, and follow-up data were examined. There were several different biochemical parameters between IAS (n=13) and B-IRS (n=6): white blood count (WBC, 7.05±3.06 vs. 2.70±0.73×109/l, p=0.004), platelet (249±56.6 vs. 111±68.0×109/l, p<0.001), serum creatine (59.0±17.8 vs. 43.1±7.05 μmol/l, p=0.013), serum albumin (42.3±5.17 vs. 33.6±3.40 g/l, p=0.002), triglyceride (median, 1.33 (1.01, 1.93) vs. 0.56 (0.50, 0.79) mmol/l, p=0.002), plasma IgG (1183±201 vs. 1832±469 mg/ml, p=0.018), IgA (328±140 vs. 469±150 mg/ml, p=0.018), and C3 (128±23.4 vs. 45.3±13.5 mg/l, p<0.001). Fasting insulin in the IAS and B-IRS patients was high (299–4708 vs. 118–851 mU/l, p=0.106), and there was a difference in 2 h oral glucose tolerance test insulin (4217–8343 mU/l vs. 274–1143 mU/l, p=0.012). Glycated hemoglobin (HbA1c) in the B-IRS patients was higher than in IAS patients (114±14.4. vs. 40.6±8.89 mmol/mol, p<0.001). Serum insulin-like growth factor-1 (IGF-1) was lower in all B-IRS patients (25±0.00 vs. 132±52.7 ng/ml, p<0.001). Although IAS and B-IRS are autoimmune hyperinsulinemic dysglycemic syndromes, several clinical parameters (body mass index, HbA1c, WBC, platelet, albumin, triglyceride, IgG, C3, and IGF-1) are different between these two syndromes.

'True' fasting serum insulin level, insulin resistance syndrome and coronary artery disease

1997 ◽  
Vol 8 (11) ◽  
pp. 683-688 ◽  
Author(s):  
Mostafa Chaour ◽  
Pierre Théroux ◽  
Brian M. Gilfix ◽  
Lucien Campeau ◽  
Jacques Lespérance ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Serum Insulin ◽  
Insulin Level ◽  
Insulin Resistance Syndrome ◽  
Serum Insulin Level ◽  
Fasting Serum ◽  
Artery Disease

FOOD CONSUMPTION AND RECTAL TEMPERATURE IN RATS DURING THIAMINE DEFICIENCY AND REPLETION

1963 ◽  
Vol 41 (12) ◽  
pp. 2463-2471 ◽  
Author(s):  
M. J. Veen ◽  
G. Russell ◽  
G. H. Beaton
Keyword(s):  
Food Consumption ◽  
Rectal Temperature ◽  
Food Restriction ◽  
Control Diet ◽  
Significant Rise ◽  
Male Rats ◽  
Thiamine Hydrochloride ◽  
Deficient Diet ◽  
Ad Libitum ◽  
Deficient Group

Rectal temperature in male rats fell slowly and gradually from ad libitum and pair-led control levels throughout a thiamine depletion period. During this period, food consumption dropped suddenly and sharply to a minimal level. A single oral dose of 50 μg of thiamine hydrochloride produced, within 4 hours, a significant rise (to less than control levels) in rectal temperature and an increase in food consumption within 24 hours. The increase in temperature was independent of the ingestion of food since diet was withheld during the 4 hours following thiamine administration. Subsequent feeding of control diet (containing thiamine) had not further increased the "4-hour" temperature after 24 hours. With continued feeding of control diet, rectal temperature rose to control levels after 3 days. On subsequent withdrawal of dietary thiamine from the deficient group, temperature and food consumption fell as before. When the animals were again repleted with 50 μg thiamine and deficient diet was continued, temperatures rose to the same level reached after the first thiamine administration. A third deprivation and repletion produced identical results.Food restriction alone, in pair-fed control groups, induced an initial elevation of rectal temperature above ad libitum control levels as temperatures in the deficient group were falling, and an eventual decrease below ad libitum control levels only after prolonged food restriction. It is suggested that the initial fall in body temperature in thiamine-deficient rats is not simply a terminal result of food restriction per se, but may reflect alterations in metabolism due to the deficiency.

scholarly journals Magnesium and calcium deficiencies additively increase zinc concentrations and metallothionein expression in the rat liver

2012 ◽  
Vol 109 (3) ◽  
pp. 425-432 ◽  
Author(s):  
Megumi Kotani ◽  
Ki Hyun Kim ◽  
Natsumi Ishizaki ◽  
Masayuki Funaba ◽  
Tohru Matsui
Keyword(s):  
Rat Liver ◽  
Control Diet ◽  
Mrna Level ◽  
Male Rats ◽  
Mrna Levels ◽  
Deficient Diet ◽  
Mg Deficiency ◽  
Ca Deficiency ◽  
Zn Concentration ◽  
Dietary Treatments

Mg deficiency increases the concentration of Zn in the liver. We investigated the effect of Mg deficiency on the expression of Zn-regulating factors such as Zn transporters and metallothionein (MT) in the rat liver. Because Ca deficiency alleviates some of the effects of Mg deficiency, we also investigated the interactions associated with Ca and Mg deficiencies. Growing male rats were given a control diet, a Mg-deficient diet, a Ca-deficient diet and a Mg- and Ca-deficient diet for 3 weeks. Mg and Ca deficiencies additively increased the mRNA levels of MT-1 and MT-2, the MT protein concentration and the concentration of Zn in the liver. The hepatic mRNA level of Zip14 increased with Mg deficiency but not with Ca deficiency. The dietary treatments did not affect the mRNA levels of other Zn transporters such as Zip1, Zip5, ZnT1, ZnT5 and ZnT6 in the liver. Ca deficiency was found to decrease the amount of femoral Zn and increase serum Zn concentration. This did not occur in the case of Mg deficiency. These results suggest that Mg deficiency enhances hepatic Zn uptake by the up-regulation of Zip14 expression and increases hepatic Zn concentration, leading to the enhancement of MT expression. Ca deficiency causes a transfer of Zn from the bone to the liver, which increases hepatic Zn concentration and, in turn, up-regulates the expression of MT. Because Mg and Ca deficiencies increase hepatic Zn concentration and increase MT expression by different mechanisms, their effects are additive.

scholarly journals Insulin resistance and impaired fat tolerance in men with coronary heart disease and ideal body weight

2004 ◽  
Vol 50 (5) ◽  
pp. 27-32
Author(s):  
I. V. Dvoryashina ◽  
N. T. Starkova ◽  
A. B. Antonov ◽  
Yu. Yu. Monogarova
Keyword(s):  
Insulin Resistance ◽  
Coronary Heart Disease ◽  
Body Weight ◽  
Heart Disease ◽  
Ideal Body Weight ◽  
Insulin Resistance Syndrome ◽  
Control Group ◽  
Blood Levels ◽  
Fatty Tissue ◽  
Ideal Body

Hormonal and metabolic disorders underlie the development of coronary heart disease (CHD). Insulin resistance, hyperinsulinemia, dyslipdemia and frequently obesity play a particular role in the pathogenesis of this disease. The purpose of this study was to characterize the basic parameters of the metabolic insulin resistance syndrome in males with CHD and an ideal body weight. A hundred and fifty-eight males were examined. They were divided into 3 groups: 1) patients with CHD and an ideal body weight; 2) those with CHD and obesity; and 3) males without CHD and obesity (a control group). The patients underwent athropometric studies; computed tomography was performed to determine the volume of abdominal fatty tissue; the blood levels of glucose, insulin, and lipids were measured. Dietary food load tests were used to study the functional activity of the lipid-transport system. Group 1 patients were found to have the major signs of the metabolic insulin-resistance syndrome: basal and stimulated hyperinsulinemia, dyslipidemia, the increased volume of visceral fatty tissue, and impaired fat tolerance.

Adequate or elevated dietary folate does not ameliorate the reduced antioxidant capacity induced by vitamin B12 deficiency in aged rats

2020 ◽  
Vol 90 (3-4) ◽  
pp. 239-248
Author(s):  
Natalia Úbeda ◽  
Teresa Partearroyo ◽  
Gregorio Varela-Moreiras
Keyword(s):  
Antioxidant Capacity ◽  
Total Antioxidant Capacity ◽  
Control Diet ◽  
Elevated Serum ◽  
Control Group ◽  
Vitamin B ◽  
Aged Rats ◽  
Sprague Dawley ◽  
Deficient Diet ◽  
Total Antioxidant

Abstract. Folate could have an antioxidant role but also may be detrimental under vitamin B12 deficiency. The aim was to investigate the effect of different dietary folic acid (FA) levels, on oxidative stress in B12 induced deficient aged rats. Thirty-five male aged Sprague–Dawley rats, were fed either a vitamin B12 deficient (n = 27) or a control diet (n = 8) during eight weeks. Then, animals were divided into four groups: B12 and FA deficient diet (DBDF), B12 deficient diet and FA control diet (DBCF), B12 deficient diet and FA supplemented diet (DBSF), and control diet (CBCF) for a 30 days period. Methionine metabolism and antioxidant status were evaluated. Both vitamins deficiencies elevated serum homocysteine (Hcy) (7.7 vs. 4.3 μmol/L, p < 0.05) and reduced S-adenosylmethionine hepatic content (283.7 vs. 581.9 μg/g protein, p < 0.05), the total antioxidant capacity (155.7 vs. 189.3 μmol/L, p < 0.05), glutathione (GSH) (120.5 vs. 419.9 μg/mg protein, p < 0.05) and oxidized glutathione (0.9 vs. 2.6 μg/mg protein, p < 0.05) compared to control. Activities of glutathione peroxidase and glutathione reductase enzymes or damage to macromolecules were unaffected. Adequate or elevated dietary FA in B12 deficiency rats decreased Hcy (5.7 and 6.3 μmol/L, respectively) and increased total antioxidant capacity (189.8 and 192.6 μmol/L, respectively) to values similar to control group, whereas GSH concentration was significantly lower than control (209.1 and 208.0 μg/mg protein respectively, p < 0.05). In conclusion, in a vitamin B12 deficiency status, adequate or elevated FA prevented impairment in one-carbon metabolism, but does not fully reverse the decrease in antioxidant capacity.

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