scholarly journals Ovariectomy is associated with metabolic impairments and enhanced mammary tumor growth in MKR mice

2015 ◽  
Vol 227 (3) ◽  
pp. 143-151 ◽  
Author(s):  
Sarit Ben-Shmuel ◽  
Eyal J Scheinman ◽  
Rola Rashed ◽  
Zila Shen Orr ◽  
Emily J Gallagher ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Mammary Tumor ◽  
Mammary Cancer ◽  
Female Mice ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Mammary Tumor Growth

Obesity and type 2 diabetes (T2D) are associated with an increased risk of breast cancer incidence and mortality. Common features of obesity and T2D are insulin resistance and hyperinsulinemia. A mammary tumor promoting effect of insulin resistance and hyperinsulinemia was demonstrated in the transgenic female MKR mouse model of pre-diabetes inoculated with mammary cancer cells. Interestingly, in MKR mice, as well as in other diabetic mouse models, males exhibit severe hyperglycemia, while females display insulin resistance and hyperinsulinemia with only a mild increase in blood glucose levels. This gender-specific protection from hyperglycemia may be attributed to estradiol, a key player in the regulation of the metabolic state, including obesity, glucose homeostasis, insulin resistance, and lipid profile. The aim of this study was to investigate the effects of ovariectomy (including the removal of endogenous estradiol) on the metabolic state of MKR female mice and subsequently on the growth of Mvt-1 mammary cancer cells, inoculated into the mammary fat pad of ovariectomized mice, compared with sham-operated mice. The results showed an increase in body weight, accompanied by increased fat mass, elevated blood glucose levels, and hypercholesterolemia, in ovariectomized MKR mice. In addition, mammary tumor growth was significantly higher in these mice. The results suggest that ovarian hormone deficiency may promote impaired metabolic homeostasis in the hyperinsulinemic MKR female mice, which in turn is associated with an increased growth of mammary tumors.

scholarly journals Efek Hipoglikemik Kecambah Beras Merah pada Tikus yang Diinduksi STZ-NA dengan Parameter Kadar Insulin, Indeks HOMA-IR dan HOMA β (Hypoglycemic Effect of Red Rice Germ on Insulin Levels, HOMA-IR, and HOMA β Index of STZ-NA Induced Rats)

2017 ◽  
Vol 36 (4) ◽  
pp. 433
Author(s):  
Nurhidajah Nurhidajah ◽  
Nurrahman Nurrahman
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Insulin Level ◽  
Control Group ◽  
Standard Diet ◽  
Red Rice ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Post Test ◽  
Decrease Blood Glucose

The process of germination of grains such as rice, could increase some nutritional values of  amino acids and dietary fiber. Red rice and its sprouts are believed to be able to decrease blood glucose in patients with diabetes mellitus (DM). The aim of this study was to evaluate the hypoglycemic effect of red rice sprouts in STZ-NA induced diabetic rats on blood glucose level, insulin level, and HOMA-IR and HOMA-β index. This experimental study was conducted based on randomized post test only control group design using 24 male Wistar rats aged 2.5 months. Rats were divided into 4 groups, one group without induction of STZ-NA fed with a standard diet (control) and three groups of STZ- NA induced with a standard diet, red rice and red rice germ. Experiments were conducted for 6 weeks. The results showed that sprouted red rice lowered blood glucose levels by 61.88 % and the value of HOMA-IR (insulin resistance parameters) by 56.82%. Insulin level increased by 16.35 % and HOMA-β by 763.6 %. This study showed that red rice germ was able to decrease blood glucose levels and increase insulin resistance of DM rats and the strength of the pancreatic beta cells. ABSTRAKProses perkecambahan biji-bijian seperti beras, dapat meningkatkan beberapa nilai gizi seperti asam amino dan serat pangan. Beras merah dan kecambahnya diyakini mampu menurunkan glukosa darah pada penderita diabetes melitus (DM). Tujuan penelitian ini adalah mengevaluasi efek hipoglikemik kecambah beras merah pada tikus diabetes yang diinduksi STZ-NA terhadap kadar glukosa darah, insulin, serta indeks HOMA-IR dan HOMA β. Penelitian ini bersifat eksperimental in vivo pada hewan coba tikus Wistar jantan usia 2,5 bulan sebanyak 24 ekor dengan desain penelitian randomized post test only control group. Tikus dibagi menjadi 4 kelompok, masing-masing 1 kelompok tanpa induksi STZ-NA dengan diet standar dan 3 kelompok diinduksi STZ-NA dengan diet standar, beras merah dan kecambah beras merah. Percobaan dilakukan selama 6 minggu. Hasil penelitian menunjukkan kecambah beras merah mampu menurunkan kadar glukosa darah sebesar 61,88 % dan nilai HOMA-IR (parameter resistensi insulin) 56,82 %. Kadar insulin meningkat 16,35 % dan HOMA β 763,6 %. Disimpulkan, kecambah beras merah mampu menurunkan kadar glukosa darah dan memperbaiki kondisi resistensi insulin tikus DM, dan kekuatan sel beta pankreas.

scholarly journals Gambaran Kadar Glukosa Darah Sewaktu Pada Penderita Hipertensi di Puskesmas II Mendoyo

2021 ◽  
Vol 10 (2) ◽  
pp. 75
Author(s):  
I Gusti Agung Dewi Sarihati ◽  
Putu Dita Pratiwi ◽  
I Gusti Agung Ayu Putu Swastini
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Blood Glucose ◽  
Data Collection ◽  
Quantitative Method ◽  
Sampling Technique ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Average Blood Glucose ◽  
Diabetes Melitus

<p class="normal" align="center"><strong>Description </strong><strong>o</strong><strong>f Blood Glucose Levels </strong><strong>i</strong><strong>n Hypertension Patients </strong><strong>in</strong><strong> Mendoyo Public </strong><strong>H</strong><strong>ealth </strong><strong>C</strong><strong>enter</strong></p><p class="normal" align="center"> </p><p class="normal"><strong> Abstract</strong></p><p class="normal"> </p><p>Hypertension is a degenerative disease that still affects many people in Bali Province. Hypertension occurs due to many factors where it can start from genetics and lifestyle. Hypertension can lead to insulin resistance which is the main cause of increased blood glucose, so that people who suffer from hypertension have the risk of suffering from diabetes mellitus. The purpose of this study is to describe the current blood glucose levels in  patients with hypertension at Puskesmas II Mendoyo. Method this research  uses descriptive quantitative method involving 30 respondents through purposive sampling technique. The research was conducted in March - April 2021. Data collection was carried out by filling out questionnaires and examining blood glukose level with POCT EasyTouch GCU. The results showed that (13.3%) patients with hypertension had blood glucose levels in the non-DM category, (80%) with the uncertain DM category, and (6.7%) in the DM category. The average blood glucose level is 120.7 mg/dl with the lowest level is 84 mg/dl and the highest level up to 273 mg/dl. In conclusion, most patients with hypertension have blood glucose levels during the uncertain DM category.</p><p><strong>Keyword</strong>s: blood glucose levels; hypertension; diabetes melitus</p>

scholarly journals Suppression of Prolactin Secretion Partially Explains the Antidiabetic Effect of Bromocriptine in ob/ob Mice

Endocrinology ◽  
2018 ◽  
Vol 160 (1) ◽  
pp. 193-204 ◽  
Author(s):  
Isadora C Furigo ◽  
Miriam F Suzuki ◽  
João E Oliveira ◽  
Angela M Ramos-Lobo ◽  
Pryscila D S Teixeira ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Insulin Sensitivity ◽  
Glucose Homeostasis ◽  
Prolactin Secretion ◽  
Dopamine Receptor Agonist ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Insulin Tolerance ◽  
Promising Therapeutic Approach

Abstract Previous studies have shown that bromocriptine mesylate (Bromo) lowers blood glucose levels in adults with type 2 diabetes mellitus; however, the mechanism of action of the antidiabetic effects of Bromo is unclear. As a dopamine receptor agonist, Bromo can alter brain dopamine activity affecting glucose control, but it also suppresses prolactin (Prl) secretion, and Prl levels modulate glucose homeostasis. Thus, the objective of the current study was to investigate whether Bromo improves insulin sensitivity via inhibition of Prl secretion. Male and female ob/ob animals (a mouse model of obesity and insulin resistance) were treated with Bromo and/or Prl. Bromo-treated ob/ob mice exhibited lower serum Prl concentration, improved glucose and insulin tolerance, and increased insulin sensitivity in the liver and skeletal muscle compared with vehicle-treated mice. Prl replacement in Bromo-treated mice normalized serum Prl concentration without inducing hyperprolactinemia. Importantly, Prl replacement partially reversed the improvements in glucose homeostasis caused by Bromo treatment. The effects of the Prl receptor antagonist G129R-hPrl on glucose homeostasis were also investigated. We found that central G129R-hPrl infusion increased insulin tolerance of male ob/ob mice. In summary, our findings indicate that part of Bromo effects on glucose homeostasis are associated with decrease in serum Prl levels. Because G129R-hPrl treatment also improved the insulin sensitivity of ob/ob mice, pharmacological compounds that inhibit Prl signaling may represent a promising therapeutic approach to control blood glucose levels in individuals with insulin resistance.

Abstract 13039: Loss of Visceral Adipose Tissue Macrophage Subsets Induces Myocardial Infarction Induced Insulin Resistance: Role of Adiponectin

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Sathish Babu B Vasamsetti ◽  
xinyi zhang ◽  
Emillie M Coppin ◽  
Jonathan Florentin ◽  
Sasha Koul ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Blood Glucose ◽  
Visceral Adipose Tissue ◽  
Fasting Blood Glucose ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Systemic Insulin Resistance ◽  
Visceral Adipose

Introduction: Myocardial infarction (MI) is the major cause of morbidity and mortality in the western world. Insulin resistance is a major complication in patients with MI. Hypothesis: Loss of visceral adipose tissue (VAT) resident macrophages in MI results in diminished adiponectin production causing systemic insulin resistance. Methods: To understand if MI results in insulin resistance, we analyzed UPMC patient records and identified patients who had normal fasting blood glucose levels on average 15 days before ST elevation myocardial infarction (STEMI) and checked their fasting blood glucose levels 30 days after STEMI. To understand the mechanisms of MI-induced insulin resistance, we used a mouse model of coronary ligation in C57BL/6 mice and analyzed the features of insulin resistance by measuring serum insulin, serum adiponectin, AKT activation status in the liver and muscle. Results: We found that 50% of non-diabetic patients (fasting blood glucose levels 99±2.5 mg/ dl) developed hyperglycemia (141±13 mg/dl) after MI, suggesting that MI causes insulin resistance. Consistently, mice with MI had higher fasting blood insulin, and reduced p-Akt levels in the liver and skeletal muscles confirming insulin resistance. Concomitantly, mice and patients with MI had reduced number of visceral adipose tissue (VAT) resident macrophages. In line with this, MI resulted in marked reduction in the level of macrophage colony stimulating factor (M-CSF), a cytokine required for tissue resident macrophage survival. M-CSF supplementation in mice with MI improved insulin sensitivity and decreased inflammatory phenotype of VAT macrophages. Furthermore, the systemic level of adiponectin, which is reported to augment insulin sensitivity, was profoundly reduced in mice after MI. Specific depletion of VAT resident macrophages resulted in lower levels of adiponectin in the serum, indicating that this macrophage subset is necessary for adiponectin production by adipocytes. Conclusions: Our data demonstrate that diminished M-CSF levels after MI triggers apoptosis of VAT resident macrophages, resulting in reduced adiponectin secretion and systemic insulin resistance.

scholarly journals Cell Autonomous Dysfunction and Insulin Resistance in Pancreatic α Cells

2019 ◽  
Vol 20 (15) ◽  
pp. 3699 ◽  
Author(s):  
Norikiyo Honzawa ◽  
Kei Fujimoto ◽  
Tadahiro Kitamura
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Blood Glucose ◽  
Current Knowledge ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Hepatic Glucose

To date, type 2 diabetes is considered to be a “bi-hormonal disorder” rather than an “insulin-centric disorder,” suggesting that glucagon is as important as insulin. Although glucagon increases hepatic glucose production and blood glucose levels, paradoxical glucagon hypersecretion is observed in diabetes. Recently, insulin resistance in pancreatic α cells has been proposed to be associated with glucagon dysregulation. Moreover, cell autonomous dysfunction of α cells is involved in the etiology of diabetes. In this review, we summarize the current knowledge about the physiological and pathological roles of glucagon.

scholarly journals Bone marrow stromal antigen 2 expressed in cancer cells promotes mammary tumor growth and metastasis

2014 ◽  
Vol 16 (6) ◽  
Author(s):  
Wadie D Mahauad-Fernandez ◽  
Kris A DeMali ◽  
Alicia K Olivier ◽  
Chioma M Okeoma
Keyword(s):  
Bone Marrow ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Mammary Tumor ◽  
Mammary Tumor Growth ◽  
Tumor Growth And Metastasis

scholarly journals Progressive development of insulin resistance phenotype in male mice with complete aromatase (CYP19) deficiency

2003 ◽  
Vol 176 (2) ◽  
pp. 237-246 ◽  
Author(s):  
K Takeda ◽  
K Toda ◽  
T Saibara ◽  
M Nakagawa ◽  
K Saika ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Serum Triglyceride ◽  
Male Mice ◽  
Wild Type ◽  
Glucose Levels ◽  
Cholesterol Levels ◽  
Blood Glucose Levels ◽  
Body Weights

Aromatase (CYP19) is a cytochrome P450 enzyme that catalyzes the formation of aromatic C18 estrogens from C19 androgens. It is expressed in various tissues and contributes to sex-specific differences in cellular metabolism. We have generated aromatase-knockout (ArKO) mice in order to study the role of estrogen in the regulation of glucose metabolism. The mean body weights of male ArKO (-/-) mice (n=7) and wild-type littermates (+/+) (n=7) at 10 and 12 weeks of age were 26.7+/-1.9 g vs 26.1+/-0.8 g and 28.8+/-1.4 g vs 26.9+/-1.0 g respectively. The body weights of the ArKO and wild-type mice diverged between 10 and 12 weeks of age with the ArKO males weighing significantly more than their wild-type littermates (P<0.05). The ArKO males showed significantly higher blood glucose levels during an intraperitoneal glucose tolerance test compared with wild-type littermates beginning at 18 weeks of age. By 24 weeks of age, they had higher fasting blood glucose levels compared with wild-type littermates (133.8+/-22.8 mg/dl vs 87.8+/-20.3 mg/dl respectively; P<0.01). An intraperitoneal injection of insulin (0.75 mU insulin/g) caused a continuous decline in blood glucose levels in wild-type mice whereas ArKO males at 18 weeks and older exhibited a rebound increase in glucose levels 30 min after insulin injection. Thus, ArKO male mice appear to develop glucose intolerance and insulin resistance in an age-dependent manner. There was no difference in fasting serum triglyceride and total cholesterol levels between ArKO male mice and wild-type littermates at 13 and 25 weeks of age. However, serum triglyceride and cholesterol levels were significantly elevated following a meal in ArKO mice at 36 weeks of age. Serum testosterone levels in ArKO male mice were continuously higher compared with wild-type littermates. Treatment of ArKO males with 17beta-estradiol improved the glucose response as measured by intraperitoneal glucose and insulin tolerance tests. Treatment with fibrates and thiazolidinediones also led to an improvement in insulin resistance and reduced androgen levels. As complete aromatase deficiency in man is associated with insulin resistance, obesity and hyperlipidemia, the ArKO mouse may be a useful animal model for examining the role of estrogens in the control of glucose and lipid homeostasis.

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