Disease Prevention through Lifestyle: A Case of the Copper to Zinc Ratio and Insulin Sensitivity

2021 ◽  
Vol 3 (2) ◽  
Author(s):  
Purnendu Nath ◽  
Sukhpreet Patel
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
High Ratio ◽  
Lifestyle Changes ◽  
Multiple Organs ◽  
High Copper

Both type 2 diabetes mellitus and a high ratio of copper to zinc are independently associated with comorbidities involving multiple organs. Separately, patients with poor insulin sensitivity are often reported as having high copper and low zinc. This article reports the case of a 46-year-old male patient interested in reversing his insulin resistance and high copper to zinc ratio, therefore reducing his long-term risk of Alzheimer’s disease. Over a period of 16 weeks, through lifestyle changes and controlling for copper in the patient’s food and water supply, the patient’s copper to zinc ratio improved from 1.91 to a healthy level of 0.55 and his HOMA-IR score improved from 2.0 to a nondiabetic level of 1.2.

scholarly journals In middle-aged siblings of patients with type 2 diabetes mellitus normal glucose tolerance is associated with insulin resistance and with increased insulin secretion. The SPIDER study

2000 ◽  
pp. 681-686 ◽  
Author(s):  
AE Pontiroli ◽  
LD Monti ◽  
S Costa ◽  
PE Sandoli ◽  
A Pizzini ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Normal Glucose Tolerance ◽  
C Peptide ◽  
Type 2 Dm ◽  
Normal Glucose

OBJECTIVES: To evaluate the frequency of impaired glucose tolerance (IGT) and of Type 2 diabetes mellitus (Type 2 DM) in siblings of patients with Type 2 DM, and to assess insulin release and insulin sensitivity in siblings with normal glucose tolerance (NGT), compared with NGT spouses of probands without family history of Type 2 DM. DESIGN AND METHODS: We evaluated 87 families including 103 Type 2 DM patients (87 probands), and we carried out an oral glucose tolerance test (OGTT) in 130 siblings and in 60 spouses. Among NGT subjects, 12 siblings and 16 spouses underwent a low-dose insulin-glucose infusion test (LDIGIT) to evaluate C-peptide release and insulin sensitivity. RESULTS: After the OGTT, 24 siblings were classified as having Type 2 DM, 31 as IGT, and only 14 spouses as IGT (P=0.0012 vs siblings). NGT siblings (n=75) showed higher insulin levels at 120 min than NGT spouses (n=46) at OGTT, in spite of identical blood glucose levels; at LDIGIT, NGT siblings secreted more C-peptide and showed a lower insulin sensitivity than NGT spouses. CONCLUSIONS: These data indicate that middle-aged siblings of probands with Type 2 DM have a high frequency of IGT and Type 2 DM, and that NGT siblings have increased insulin resistance and increased insulin secretion when compared with adequate controls.

Long-term effects of pioglitazone and metformin on insulin sensitivity in patients with Type 2 diabetes mellitus

2005 ◽  
Vol 22 (8) ◽  
pp. 1101-1106 ◽  
Author(s):  
M. Roden ◽  
M. Laakso ◽  
D. Johns ◽  
M. Widel ◽  
R. Urquhart ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Insulin Sensitivity ◽  
Long Term Effects

scholarly journals N1-Methylnicotinamide Improves Hepatic Insulin Sensitivity via Activation of SIRT1 and Inhibition of FOXO1 Acetylation

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Jingfan Zhang ◽  
Yu Chen ◽  
Cong Liu ◽  
Ling Li ◽  
Ping Li
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Blood Glucose ◽  
Insulin Sensitivity ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Related Proteins

Objective. To explore the effects of N1-methylnicotinamide (MNAM) on insulin resistance and glucose metabolism in obese type 2 diabetes mellitus (T2DM) mice and regulatory mechanisms of the NAD-dependent deacetylase sirtuin-1 (SIRT1)/forkhead box protein O1 (FOXO1) pathway. Methods. Blood glucose and insulin levels were examined in mice. HE and oil red O staining were used to observe the effects of MNAM on liver lipid deposition in ob/ob mice. Real-time PCR and Western blotting were used to detect expression of gluconeogenesis, insulin signaling-related proteins, and SIRT1/FOXO1 pathway-related proteins. L-O2 cells were cultured as a model of insulin resistance, and MNAM and SIRT1 inhibitors were administered in vivo. Residual glucose and insulin signaling-related proteins were detected and the mechanisms associated with the SIRT1/FOXO1 signaling pathway in insulin resistance explored. Results. MNAM can effectively reduce levels of fasting blood glucose and insulin, improve liver morphology, and reduce lipid accumulation in obese type 2 diabetes mellitus mice. MNAM also downregulates the key proteins in the gluconeogenesis pathway in the liver, upregulates Sirt1 expression, and reduces acetylation of the FOXO1 protein. In vitro, MNAM could promote the glucose uptake capacity of L-O2 cells induced by palmitic acid (PA), a saturated fatty acid that induces IR in various scenarios, including hepatocytes, improving insulin resistance. As Sirt1 expression was inhibited, the reduction of hepatocyte gluconeogenesis and the regulation of the insulin signaling pathway by MNAM were reversed. Conclusion. MNAM activates SIRT1 and inhibits acetylation of FOXO1, which in turn regulates insulin sensitivity in type 2 diabetic mice, leading to a reduction of hepatic glucose output and improvement of insulin resistance.

scholarly journals Association of Serum Magnesium Deficiency with Insulin Resistance in Type 2 Diabetes Mellitus

2015 ◽  
Vol 7 (02) ◽  
pp. 075-078 ◽  
Author(s):  
Happy Chutia ◽  
Kyrshanlang G Lynrah
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Insulin Sensitivity ◽  
Serum Magnesium ◽  
Magnesium Level ◽  
Serum Magnesium Level ◽  
Sensitivity Indices

ABSTRACT Background: Insulin resistance (IR) is the key pathophysiological defect that leads to the development of type 2 diabetes mellitus. The purpose of this study was to estimate serum magnesium level and insulin sensitivity indices among type 2 diabetes mellitus patients and to see an association between them. Methods: This study was carried out among 38 type 2 diabetic patients and forty age and sex matched controls. Serum fasting glucose, magnesium, insulin, urea, and creatinine levels were estimated. Insulin sensitivity indices, homeostasis model assessment for insulin resistance (HOMA-IR) and quantitative insulin sensitivity check index (QUICKI) levels were calculated as per formulae. Results: A highly significant low serum magnesium level was found in diabetic subjects as compared to the controls. Statistically significant high HOMA levels (>2.6) and low QUICKI levels (< 0.33) were found among the case group. An inverse, statistically significant correlation was found between serum magnesium and fasting insulin level. A highly statistically significant inverse correlation was found between serum magnesium and HOMA level, and a positive correlation was found between serum magnesium and QUICKI level, that is, serum magnesium level decreases with increase in IR. A strong association was also found between fasting serum insulin level and insulin sensitivity indices. Conclusion: This study showed a lower serum magnesium level in diabetic patients compared to control. A strong association was also found between serum magnesium level and insulin sensitivity indices. For proper management of type 2 diabetes, it may, therefore, be necessary to treat hypomagnesemia in these patients.

Methods of Measuring Insulin Sensitivity

2007 ◽  
Vol 8 (4) ◽  
pp. 305-318 ◽  
Author(s):  
Kimberly K. Trout ◽  
Carol Homko ◽  
Nancy C. Tkacs
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Biological Response ◽  
Insulin Resistant ◽  
Advantages And Disadvantages ◽  
Health Disorders

Insulin resistance is a component of several health disorders, most notably impaired glucose tolerance and type 2 diabetes mellitus. Insulin-resistant individuals have an impaired biological response to the usual action of insulin; that is, they have reduced insulin sensitivity. Various methods are used to assess insulin sensitivity both in individuals and in study populations. Validity, reproducibility, cost, and degree of subject burden are important factors for both clinicians and researchers to consider when weighing the merits of a particular method. This article describes several in vivo methods used to assess insulin sensitivity and presents the advantages and disadvantages of each.

Interferon regulatory factor 7 deficiency prevents diet-induced obesity and insulin resistance

2013 ◽  
Vol 305 (4) ◽  
pp. E485-E495 ◽  
Author(s):  
Xin-An Wang ◽  
Ran Zhang ◽  
Shumin Zhang ◽  
Shan Deng ◽  
Dingsheng Jiang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Energy Metabolism ◽  
Interferon Regulatory Factor ◽  
Type I ◽  
Regulatory Factor ◽  
Multiple Organs ◽  
Interferon Regulatory Factor 7

Obesity-related inflammation has been implicated in the pathogenesis of insulin resistance and type 2 diabetes. In this study, we addressed the potential role of interferon regulatory factor 7 (IRF7), a master regulator of type I interferon-dependent immune responses, in the regulation of energy metabolism. The expression levels of IRF7 were increased in white adipose tissue, liver tissue, and gastrocnemius muscle of both diet-induced obese mice and ob/ ob mice compared with their lean counterparts. After feeding a high-fat diet (HFD) for 24 wk, IRF7 knockout (KO) mice showed less weight gain and adiposity than wild-type controls. KO of IRF7 improved glucose and lipid homeostasis and insulin sensitivity. Additionally, KO of IRF7 ameliorated diet-induced hepatic steatosis. Next, we assessed the inflammatory state of the IRF7 KO mice on the HFD. These mice showed less macrophage infiltration into multiple organs and were protected from local and systemic inflammation. This study demonstrates a role for IRF7 in diet-induced alterations in energy metabolism and insulin sensitivity. Our results also suggest that IRF7 is involved in the etiology of metabolic abnormalities, which suggests a new strategy for treating obesity and type 2 diabetes.

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