【中国的糖尿病】

 

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http://www.thelancet.com/pb/assets/raw/Lancet/stories/series/diabetes-in-china-series2-chinese.pdf

 

中国是全球糖尿病 患者最多的国家，超过1亿多成人患有此病，约占总人口的 12%，而且还在增长。

中国成年人群中糖尿病前期（Impaired glucose tolerance, IGT）患病率为50.1%。WHO 资料显示 中国近半数成年人处于糖尿病前期，约为5亿人。

在对日本患者的口服葡萄糖试验中，发现胰岛素分泌量较低，而胰岛素抵抗只是次要因素。 在经过挑选的体型偏瘦的中国II-型糖尿病患者身上测到了较低的C-肽（C-peptide）水平，显示胰岛素分泌不足。

这个测试的结论显示：对中国的II-型患者而言，较瘦者的主要病因是胰岛素分泌能力不足，而较胖者的病因则兼有胰岛素抵抗。

2004年，美国新泽西医学院的医生们对三个不同族裔的妇女在胰脏β-细胞功能做了稳态模型估测（homeostasis model assessments），胰脏β-细胞的主要功能是分泌胰岛素。结果发现非洲裔妇女的胰岛素分泌能力强于欧洲裔，而欧洲裔妇女则强于东亚裔。

这个测试揭示了非洲和东亚两个人群的胰岛素分泌能力存在较大差异，前者发生糖尿病的病因主要是胰岛素抵抗，病因是不良饮食习惯。

而后者主要是胰岛素分泌量不足。2003年在日本进行的对50岁以上男性的测试中，得出了相似的结论[4]。

东亚人相对较低的胰岛素分泌功能可以找到基因上的原因。

https://www.zhihu.com/question/21789488?

Current approaches for assessing insulin sensitivity and resistance 

http://ajpendo.physiology.org/content/294/1/E15.long

In insulin resistance, muscle, fat, and liver cells do not respond properly to insulin and thus cannot easily absorb glucose from the bloodstream. As a result, the body needs higher levels of insulin to help glucose enter cells.

The beta cells in the pancreas try to keep up with this increased demand for insulin by producing more. As long as the beta cells are able to produce enough insulin to overcome the insulin resistance, blood glucose levels stay in the healthy range.

What causes insulin resistance?

Although the exact causes of insulin resistance are not completely understood, scientists think the major contributors to insulin resistance are excess weight and physical inactivity.

https://www.niddk.nih.gov/health-information/diabetes/overview/what-is-diabetes/prediabetes-insulin-resistance

Other Causes

Other causes of insulin resistance may include ethnicity; certain diseases; hormones; steroid use; some medications; older age; sleep problems, especially sleep apnea; and cigarette smoking.

 

 

Over time, insulin resistance can lead to type 2 diabetes and prediabetes because the beta cells fail to keep up with the body's increased need for insulin. Without enough insulin, excess glucose builds up in the bloodstream, leading to diabetes, prediabetes, and other serious health disorders.

 

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Role of Chromium in Human Health and in Diabetes

http://care.diabetesjournals.org/content/27/11/2741

Chromium in glucose metabolism

https://en.wikipedia.org/wiki/Chromium_in_glucose_metabolism

It is believed to interact with the low-molecular weight chromium (LMWCr) binding substance to amplify the action of insulin. 

Chromium increases insulin binding to cells, insulin receptor number and activates insulin receptor kinase leading to increased insulin sensitivity. 

https://www.ncbi.nlm.nih.gov/pubmed/10705100

 

Selenium Supplementation Improves Insulin Sensitivity And Lipids In Women With PCOS

In a clinical trial epublished in December 2014, researchers determined that selenium supplementation improved insulin metabolism, triglycerides, and very-low density lipoprotein (VLDL) cholesterol in women with polycystic ovary syndrome (PCOS). PCOS is characterized by hormone imbalances resulting in androgen excess, decreased or absent ovulation, and cystic ovaries. Women with PCOS typically have elevated lipids and approximately 40% have insulin resistance independent of body weight. The National Institutes of Health reports that between one in 10 and one in 20 women of childbearing age has PCOS, affecting up to five million women in the United States.

The subjects included 70 women diagnosed with PCOS between 18 to 40 years of age. The researchers randomly assigned the subjects to receive 200 mcg per day selenium or a placebo daily for eight weeks. The investigators evaluated blood glucose, insulin, and lipids at the beginning of the study and again after the eight-week intervention period.

After the supplementation period, the subjects in the selenium supplementation group had significantly decreased serum insulin levels, insulin resistance (homeostasis model of assessment-insulin resistance), and homeostatic model assessment-Beta-cell function compared to the placebo group. Additionally, insulin sensitivity was increased in the selenium group compared to the placebo group. Triglycerides and VLDL cholesterol also were reduced in the selenium group compared to the placebo group.

The researchers stated, "In conclusion, 200 microgram per day selenium supplementation for eight weeks among PCOS women had beneficial effects on insulin metabolism parameters, triglycerides and VLDL-C levels; however, it did not affect fasting plasma glucose and other lipid profiles."

REFERENCE:

http://www.cpmedical.net/newsletter/selenium-supplementation-improves-insulin-sensitivity-and-lipids-in-women-with-pcos

Cell Mol Life Sci. 2000 Dec;57(13-14):1874-9.

Selenium: an insulin-mimetic.

Stapleton SR1.

Author information

 

Abstract

Insulin or agents that can mimic its action (insulin-mimetics) are necessary to promote the entry of glucose into tissues where the glucose can either be converted into energy or stored for later use. In recent years, selenium has been shown to mediate a number of insulin-like actions both in vivo and in vitro. These insulin-like actions include stimulating glucose uptake and regulating metabolic processes such as glycolysis, gluconeogenesis, fatty acid synthesis and the pentose phosphate pathway. The mechanism by which selenium is capable of mimicking insulin is not clear; however, reports indicate that selenium does activate key proteins involved in the insulin-signal cascade. Various proteins in the insulin-signal cascade have been shown to be necessary for different insulin-regulated events, and presumably data will be forthcoming soon that illustrate this similarly for selenium. This review compares the action of selenium to that of insulin and discusses the available evidence in support of selenium as an insulin-mimetic.

PMID:

 

11215514

 

DOI:

 

10.1007/PL00000669

[PubMed - indexed for MEDLINE]

 

https://www.ncbi.nlm.nih.gov/pubmed/11215514

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Insulin promotes glucose and amino acid uptake, lipogenesis, intracellular transport, and the synthesis of proteins and nucleic acids. Transferrin is an iron carrier and it may also help to reduce toxic levels of oxygen radicals and peroxide. Selenium, as sodium selenite, is a co-factor for glutathione peroxidase and other proteins, and is used as an anti-oxidant in media.

https://www.thermofisher.com/order/catalog/product/41400045

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Horm Metab Res. 2016 Apr;48(4):263-8. doi: 10.1055/s-0035-1569276. Epub 2016 Jan 7.

Selenium Supplementation Affects Insulin Resistance and Serum hs-CRP in Patients with Type 2 Diabetes and Coronary Heart Disease.

Farrokhian A1, Bahmani F2, Taghizadeh M2, Mirhashemi SM2, Aarabi MH2, Raygan F1, Aghadavod E2, Asemi Z2.

Author information

 

Abstract

To our knowledge, this study is the first indicating the effects of selenium supplementation on metabolic status of patients with type 2 diabetes mellitus (T2DM) and coronary heart disease (CHD). This study was conducted to evaluate the effects of selenium supplementation on metabolic profiles, biomarkers of inflammation, and oxidative stress of patients with T2DM and CHD. This randomized, double-blind, placebo-controlled trial was performed among 60 patients with T2DM and CHD aged 40-85 years. Participants were randomly divided into 2 groups. Group A received 200 μg selenium supplements (n=30) and group B received placebo per day (n=30) for 8 weeks. Fasting blood samples were taken at the beginning of the study and after 8-week intervention to quantify metabolic profiles. After 8 weeks, compared with the placebo, selenium supplementation resulted in a significant decrease in serum insulin levels (- 2.2±4.6 vs. + 3.6±8.4 μIU/ml, p=0.001), homeostasis model of assessment-insulin resistance (HOMA-IR) (- 0.7±1.3 vs. + 0.9±2.4, p=0.004), homeostatic model assessment-beta cell function (HOMA-B) (- 7.5±17.2 vs. + 15.1±34.5, p=0.002) and a significant increase in quantitative insulin sensitivity check index (QUICKI) (+0.01±0.03 vs. - 0.01±0.03, p=0.02). In addition, patients who received selenium supplements had a significant reduction in serum high-sensitivity C-reactive protein (hs-CRP) (- 1 372.3±2 318.8 vs. - 99.8±1 453.6 ng/ml, p=0.01) and a significant rise in plasma total antioxidant capacity (TAC) concentrations (+ 301.3±400.6 vs. - 127.2±428.0 mmol/l, p<0.001) compared with the placebo. A 200 μg/day selenium supplementation among patients with T2DM and CHD resulted in a significant decrease in insulin, HOMA-IR, HOMA-B, serum hs-CRP, and a significant increase in QUICKI score and TAC concentrations.

© Georg Thieme Verlag KG Stuttgart · New York.

PMID:

 

26743526

 

DOI:

 

10.1055/s-0035-1569276

 

https://www.ncbi.nlm.nih.gov/pubmed/26743526

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Chromium picolinate  alleviating insulin resistance

glucose-tolerance factor (GTF) chromium and chromium picolinate.

The insulin receptor is a member of the ligand-activated receptor and tyrosine kinase family of transmembrane signaling proteins that collectively are fundamentally important regulators of cell differentiation, growth, and metabolism. The insulin receptor has a number of unique physiological and biochemical properties.

https://www.ncbi.nlm.nih.gov/pubmed/8141246

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3308119/

 

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Met Ions Biol Syst. 1995;31:575-94.

Vanadium compounds as insulin mimics.

Orvig C1, Thompson KH, Battell M, McNeill JH.

Author information

 

Abstract

That vanadium compounds act in an insulin-mimetic fashion both in vitro and in vivo has been well established. Both inorganic and organic vanadium compounds have been shown to lower plasma glucose levels, increase peripheral glucose uptake, improve insulin sensitivity, decrease plasma lipid levels, and normalize liver enzyme activities in a variety of animal models of both type I and type II diabetes. Vanadium treatment of diabetic animals does not restore plasma insulin levels but may spare pancreatic insulin. Elucidation of the mechanism(s) of action and potentiation of vanadium's insulin-mimetic effect by appropriate ligand binding would seem to be the highest priorities for future investigation.

https://www.ncbi.nlm.nih.gov/pubmed/8564818

 

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