Beneficial role of vitamin K supplementation on insulin sensitivity, glucose metabolism, and the reduced risk of type 2 diabetes: A review

Nutrition ◽  
2016 ◽  
Vol 32 (7-8) ◽  
pp. 732-739 ◽  
Author(s):  
Prasenjit Manna ◽  
Jatin Kalita
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Vitamin K ◽  
Beneficial Role ◽  
Reduced Risk

scholarly journals Adipocyte PU.1 knockout promotes insulin sensitivity in HFD-fed obese mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Denise E. Lackey ◽  
Felipe C. G. Reis ◽  
Roi Isaac ◽  
Rizaldy C. Zapata ◽  
Dalila El Ouarrat ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Target Genes ◽  
Obese Mice ◽  
Tissue Macrophage

Abstract Insulin resistance is a key feature of obesity and type 2 diabetes. PU.1 is a master transcription factor predominantly expressed in macrophages but after HFD feeding PU.1 expression is also significantly increased in adipocytes. We generated adipocyte specific PU.1 knockout mice using adiponectin cre to investigate the role of PU.1 in adipocyte biology, insulin and glucose homeostasis. In HFD-fed obese mice systemic glucose tolerance and insulin sensitivity were improved in PU.1 AKO mice and clamp studies indicated improvements in both adipose and liver insulin sensitivity. At the level of adipose tissue, macrophage infiltration and inflammation was decreased and glucose uptake was increased in PU.1 AKO mice compared with controls. While PU.1 deletion in adipocytes did not affect the gene expression of PPARg itself, we observed increased expression of PPARg target genes in eWAT from HFD fed PU.1 AKO mice compared with controls. Furthermore, we observed decreased phosphorylation at serine 273 in PU.1 AKO mice compared with fl/fl controls, indicating that PPARg is more active when PU.1 expression is reduced in adipocytes. Therefore, in obesity the increased expression of PU.1 in adipocytes modifies the adipocyte PPARg cistrome resulting in impaired glucose tolerance and insulin sensitivity.

scholarly journals Habenula lesions improve glucose metabolism in rats with type 2 diabetes by increasing insulin sensitivity and inhibiting gluconeogenesis

2020 ◽  
Vol 8 (1) ◽  
pp. e001250
Author(s):  
Peng Qu ◽  
Yachun Wang ◽  
Lei Liu ◽  
Mengmeng Qi ◽  
Yimeng Sun ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Nervous System ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Sham Group ◽  
Adrenal Glands ◽  
Tolerance Test ◽  
Lesion Group

IntroductionThe habenular nucleus (Hb), a famous relay station in the midbrain, is vital for controlling many physiological functions of vertebrates. The role of Hb in the pathogenesis of depression has been thoroughly studied, but whether it functions in the pathogenesis of diabetes remains unknown. In this study, we found that Hb lesions could improve glucose metabolism in type 2 diabetes mellitus (T2DM) by inhibiting the peripheral sympathetic nervous system and hepatic glucose production.Research design and methodsT2DM rats were induced by a high-carbohydrate and fat diet combined with streptozotocin. Electrical lesion method was applied to suppress the function of Hb. Serum and tissue samples of rats in the control group, T2DM group, sham group, and Hb lesion group were detected by ELISA, western blotting, and biochemical methods.ResultsCompared with the sham group, the expression levels of AMPK phosphorylation and insulin receptor (IR) were significantly increased, whereas glucose-6-phosphatase and phosphoenolpyruvate carboxylated kinase were reduced in the liver of the Hb lesion group. In the glucose tolerance test and pyruvate tolerance test, the lesion group showed stronger glucose tolerance and lower hepatic gluconeogenesis than the sham. These results suggest that Hb lesions not only effectively increase insulin sensitivity and improve insulin resistance but also inhibit gluconeogenesis in T2DM rats. Moreover, Hb lesions increase the expression of brain-derived neurotrophic factor, tropomyosin receptor kinase B, glucocorticoid receptor, and IR in the hippocampus. In this study, we also found that Hb lesions increase the content of acetylcholine in the adrenal glands and reduce the content of epinephrine in both the adrenal glands and the liver, which may be the main reason for the Hb lesions to regulate glucose metabolism in the liver.ConclusionHb is an important neuroanatomical target for the regulation of glucose metabolism in the central nervous system of diabetic rats.

scholarly journals Role of the renal sympathetic nerve in renal glucose metabolism during the development of type 2 diabetes in rats

Diabetologia ◽  
2015 ◽  
Vol 58 (12) ◽  
pp. 2885-2898 ◽  
Author(s):  
Kazi Rafiq ◽  
Yoshihide Fujisawa ◽  
Shamshad J. Sherajee ◽  
Asadur Rahman ◽  
Abu Sufiun ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Metabolism ◽  
Sympathetic Nerve ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Prophylactic role of vitamin K supplementation on vascular inflammation in type 2 diabetes by regulating the NF-κB/Nrf2 pathwayviaactivating Gla proteins

2018 ◽  
Vol 9 (1) ◽  
pp. 450-462 ◽  
Author(s):  
Anjum Dihingia ◽  
Dibyajyoti Ozah ◽  
Pranab Kumar Baruah ◽  
Jatin Kalita ◽  
Prasenjit Manna
Keyword(s):  
Type 2 Diabetes ◽  
Vitamin K ◽  
Vascular Inflammation ◽  
Vitamin K1 ◽  
The Relationship

There is no previous study that has examined the relationship between circulating vitamin K1 (VK1) and vascular inflammation in type 2 diabetes (T2D).

scholarly journals Effect of pistachios on lipids, lipoproteins, glucose metabolism, and insulin sensitivity in type 2 diabetes

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Katherine A Sauder ◽  
Cindy E McCrea ◽  
Penny M Kris‐Etherton ◽  
Jan S Ulbrecht ◽  
Sheila G West
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Glucose Metabolism

scholarly journals Beneficial Effects of Vitamin K Status on Glycemic Regulation and Diabetes Mellitus: A Mini-Review

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2485
Author(s):  
Hsin-Jung Ho ◽  
Michio Komai ◽  
Hitoshi Shirakawa
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Insulin Sensitivity ◽  
Vitamin K ◽  
Glycemic Status ◽  
Beneficial Effects ◽  
Onset Of Diabetes ◽  
Glycemic Regulation

Type 2 diabetes mellitus is a chronic disease that is characterized by hyperglycemia, insulin resistance, and dysfunctional insulin secretion. Glycemic control remains a crucial contributor to the progression of type 2 diabetes mellitus as well as the prevention or delay in the onset of diabetes-related complications. Vitamin K is a fat-soluble vitamin that plays an important role in the regulation of the glycemic status. Supplementation of vitamin K may reduce the risk of diabetes mellitus and improve insulin sensitivity. This mini-review summarizes the recent insights into the beneficial effects of vitamin K and its possible mechanism of action on insulin sensitivity and glycemic status, thereby suppressing the progression of diabetes mellitus.

scholarly journals The Role of Diet on Insulin Sensitivity

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3042
Author(s):  
Maria Mirabelli ◽  
Diego Russo ◽  
Antonio Brunetti
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Insulin Sensitivity ◽  
Dietary Composition ◽  
Reproductive Disorders

Growing evidence shows that dietary composition has a marked impact on the risk of developing obesity, type 2 diabetes (T2D), cardiovascular disease (CVD), certain types of endocrine cancer and many other intertwined metabolic and reproductive disorders, all featured by insulin resistance (IR) [...]

scholarly journals The effect of coffee consumption on insulin sensitivity and other biological risk factors for type 2 diabetes: a randomized placebo-controlled trial

2019 ◽  
Vol 111 (2) ◽  
pp. 448-458 ◽  
Author(s):  
Derrick Johnston Alperet ◽  
Salome Antonette Rebello ◽  
Eric Yin-Hao Khoo ◽  
Zoey Tay ◽  
Sharna Si-Ying Seah ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Controlled Trial ◽  
Coffee Consumption ◽  
Small Sample ◽  
Urinary Creatinine ◽  
Sensitivity Indices

ABSTRACT Background In observational studies, coffee consumption has been consistently associated with a lower risk of type 2 diabetes mellitus. Trials examining the effect of coffee consumption on glucose metabolism have been limited by the use of surrogate insulin sensitivity indices, small sample sizes, lack of blinding, and short follow-up duration. Objectives We aimed to overcome limitations of previously conducted coffee trials in a randomized placebo-controlled trial of the effect of coffee consumption on insulin sensitivity. Methods We conducted a 24-wk randomized placebo-controlled trial in 126 overweight, non–insulin sensitive (HOMA-IR ≥1.30), Chinese, Malay, and Asian-Indian males and females aged 35–69 y. Participants were randomly assigned to receive 4 cups of instant regular coffee (n = 62) or 4 cups of a coffee-like placebo beverage (n = 64) per day. The primary outcome was the amount of glucose metabolized per kilogram of body weight per minute (Mbw) assessed during steady-state conditions with a hyperinsulinemic euglycemic clamp. Secondary outcomes included other clamp-based insulin sensitivity measures, biological mediators of insulin sensitivity, and measures of fasting glucose metabolism. Results Coffee consumption did not significantly change insulin sensitivity compared with placebo (percentage mean difference in Mbw = 4.0%; 95% CI: −8.3, 18.0%; P = 0.53). Furthermore, no significant differences in fasting plasma glucose (2.9%; 95% CI: −0.4, 6.3%; P = 0.09) or biological mediators of insulin resistance, such as plasma adiponectin (2.3%; 95% CI: −1.4, 6.2%; P = 0.22), were observed between coffee and placebo groups over 24 wk of intervention. Participants in the coffee arm experienced a loss of fat mass (FM) (−3.7%; 95% CI: −6.3, −1.1%; P = 0.006) and reduction in urinary creatinine concentrations (−21.2%; 95% CI: −31.4, −9.5%; P = 0.001) compared with participants in the placebo arm over 24 wk of intervention. Conclusions Consuming 4 cups/d of caffeinated coffee for 24 wk had no significant effect on insulin sensitivity or biological mediators of insulin resistance but was associated with a modest loss of FM and reduction in urinary creatinine concentrations. This trial was registered at clinicaltrials.gov as NCT01738399. Registered on November 28, 2012. Trial sponsor: Nestlé Research, Lausanne, Switzerland. Trial site: National University of Singapore.

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