SUMMARYTissue cultures of onion, differentiated into roots and shoots, were examined for total flavour precursor levels, composition of the flavour precursors and activity of the enzyme alliinase. Comparisons were made with undiflerentiated callus and with the roots and shoots of germinating seedlings and shooting bulbs.Undiflerentiated callus contained none of the major flavour precursor compound, 5-transprop-1 -enyl-i.-cysteine sulphoxide, but in the diflFerentiated tissue this compound was present in both redifterentiated roots and shoots. In intact plants, more flavour precursor accumulated in rapidly growing roots and shoots.
Type II Diabetes (T2D) and insulin resistance are growing national health concerns. Obesity is a risk factor for developing T2D and is associated with chronic and systemic inflammation. Exercise on the other hand has been shown to improve glucose metabolism and insulin sensitivity. We investigated the effects of conditioning and weight gain on adiponectin, tumor necrosis factor and glycosylated hemoglobin, three biomarkers of T2D. We measured the levels of these three biomarkers in racing, sedentary and overweight sled dogs. Exercise did not have a significant impact on the levels of the biomarkers, whereas weight gain had a negative effect. Using a sled dog model, we conclude that weight management is important to reduce the risk of T2D and its consequences.
Insulin increases glucose uptake in skeletal muscle cells and adipose tissue by stimulating the recruitment of the glucose transporter 4 (Glut4) to plasma membranes from a pool of storage vesicles. Type II diabetes (T2D) is characterized by an inability to clear blood glucose in response to insulin due to an impairment of Glut4 recruitment and/or function. A persistent, systemic inflammatory and oxidative stress (IOS) is key to the impairment of insulin‐stimulated glucose uptake. Diets high in saturated fatty acids promote insulin resistance mediated by IOS and a disruption of sphingolipid metabolism. T2D incidence has reached epidemic proportions in the US population and worldwide and is strongly associated with obesity. Although the incidence of obesity in Alaska Natives is higher compared to rest of the US population, incidence of T2D is considerably less, which is largely attributed to their subsistence diet rich in Alaska berry fruits.The objective of this study is to demonstrate whether botanical extracts of wild berries endemic to Alaska harbor the potency to protect or restore insulin‐stimulated glucose uptake utilizing a cellular model of T2D.Acute insulin exposure of adipocytes and myotubes stimulates a rapid recruitment of Glut4 (glucose transporter 4) to plasma membranes thereby increasing glucose uptake. Cells under control conditions (0.1 mg/ml BSA) responded to increasing concentrations of insulin (100 nM and 200 nM) with an increase in glucose uptake (100 nM: 1.80 +0.43 %, n=8, *p<0.05 and 200 nM: 2.23 + 0.42 %, n=8, *p<0.01) utilizing 2‐NBD‐glucose (2‐(N‐(7‐Nitrobenz‐2‐oxa‐1,3‐diazol‐4‐yl)Amino)‐2‐Deoxyglucose, a fluorescent glucose reporter). In sharp contrast, pretreatment of cells with 0.75 mM palmitate (saturated C16 fatty acid adsorbed onto BSA) for 18 h significantly abolished insulin‐stimulated glucose uptake (100 nM insulin in palmitate treated cells compared to 100 nM insulin and control p<0.05). Cells pretreated with palmitate and increasing concentrations of insulin (100 nM and 200 nM) did not show a significant difference (100 nM: 1.59 +0.12 %, n=8, and 200 nM: 2.05 + 0.18 %, n=8).Conclusively, persistent presence of palmitate impairs insulin‐mediated glucose transport and plasma membrane recruitment of Glut4. Supplementation of adipocytes or skeletal myotubes with Alaskan berry botanicals (crude extracts, total anthocyanins, total proanthocyanidins) prior to addition of palmitate partially restored insulin‐stimulated glucose uptake.Support or Funding InformationResearch was supported by the National Institute Of General Medical Sciences of the National Institutes of Health under Award Numbers UL1GM118991, TL4GM118992, or RL5GM118990.Research was supported by an Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health under grant number P20GM103395.
Alaska natives were recently found to have the fastest increase in diagnosed type II diabetes (T2D) cases in the U.S. population due to the influence of western diets. A common manifestation of T2D is insulin resistance which alters the body's regulation of insulin and glucose metabolism. Alaskan blueberries have been shown to have a higher content of antioxidants in the form of anthocyanins compared to other varieties. Dietary anthocyanins have have shown to act on the insulin transduction pathway and reduce insulin resistance. Our research focuses on the anthocyanins present in Alaska wild bog blueberries and their potency to prevent and reduce insulin resistance and therefore mitigate T2D development.The experimental design encompassed differentiated 3T3‐L1 adipocytes exposed to palmitate for 16 hr, which reduces insulin‐dependent glucose uptake, in the presence or absence of anthocyanins. Our study focused on the phosphorylation of AS160, a pivotal substrate in the insulin transduction pathway, as a response of the cells to insulin. Anthocyanin fractions (ANC) (10 ug/mL) were applied for 1 hr prior to palmitate (0.75 mM, 16 h) and were present throughout the stress period. Total cell lysates were analyzed by western blotting to determine the presence of phosphorylated AS160.Each condition was run in duplicate and two western blots were run. The software ImageJ was used to obtain relative levels of p‐AS160. Values were obtained from the ratio of insulin stimulated over basal levels of AS160.The control, (no palmitate or ANCs), had the highest amount of phosphorylated AS160 (1.925, p <0.05). Cells stressed with palmitate had the least AS160 phosphorylation levels (0.791 p= 0.05). Importantly, cells treated with ANCs prior to stress exhibited 1.047 (p=0.11) of phosphorylated AS160.The data supports the hypothesis that the ANCs used prior to stressing the cells mitigates insulin resistance. Future work will look at an intervention paradigm and focus on a comparative analysis of prevention and intervention.Support or Funding InformationWork reported in this publication was supported by the National Institute of General Medical Sciences of the National Institutes of Health under three linked awards number RL5GM118990, TL4GM118992 and 1UL1GM118991. The work is solely the responsibility of the authors and does not necessarily represent the official view of the National Institutes of Health.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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