Effects of beta-cell rest on beta-cell function: a review of clinical and preclinical data

Brown, Rebecca; Rother, Kristina I.

doi:10.1111/j.1399-5448.2007.00272.x

Cited by 95 publications

(70 citation statements)

References 67 publications

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“…This finding may be explained by protection against ROS-induced beta-cell dysfunction by a fashion that differs from that in insulin sensitive peripheral tissues. In our study GLX351322 counteracted partially ROS production, high-glucose-induced islet cell death and the release of insulin in response to a high concentration of glucose in vitro, which fits well with the notion that oxidative stress is deleterious, and that beta-cell rest leads to long-term preservation of beta-cell function in vivo [35].…”

Section: Discussionsupporting

confidence: 68%

The novel NADPH oxidase 4 inhibitor GLX351322 counteracts glucose intolerance in high-fat diet-treated C57BL/6 mice

Anvari

Wikström

Walum

et al. 2015

Free Radical Research

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The novel NADPH oxidase 4 inhibitor GLX351322 counteracts glucose intolerance in high-fat diet-treated C57BL/6 mice.. (11) http://dx.doi.org/10. 3109/10715762.2015.1067697 Access to the published version may require subscription. N.B. When citing this work, cite the original published paper. EA and PW performed the experiments. PW, EW and NW designed the experiments, analyzed the results and wrote the manuscript. Free radical research, 49 2 ABSTRACTIn Type 2 diabetes, it has been proposed that pancreatic beta-cell dysfunction is promoted by oxidative stress caused by NADPH oxidase (NOX) over-activity. Five different NOX enzymes (NOX1-5) have been characterized, among which NOX1 and NOX2 have been proposed to negatively affect beta-cells, but the putative role of NOX4 in type 2 diabetes-associated beta-cell dysfunction and glucose intolerance is largely unknown. Therefore, we presently investigated the importance of NOX4 for high-fat diet (HFD)-induced glucose intolerance using male C57BL/6 mice using the new NOX4 inhibitor GLX351322, which has relative NOX4 selectivity over NOX2. In HFD-treated male C57BL/6 mice a two-week treatment with GLX351322 counteracted non-fasting hyperglycemia and impaired glucose tolerance. This effect occurred without any change in peripheral insulin sensitivity. To ascertain that NOX4 also plays a role for the function of human beta-cells, we observed that glucose-and sodium palmitate-induced insulin release from human islets in vitro was increased in response to NOX4 inhibitors. In longterm experiments (1-3 days), high glucose-induced human islet cell ROS production and death were prevented by GLX351322. We propose that whilst short-term NOX4-generated ROS production is a physiological requirement for beta-cell function, persistent NOX4-activity, e.g. during conditions of high-fat feeding, promotes ROSmediated beta-cell dysfunction. Thus, selective NOX-inhibition may be a therapeutic strategy in Type 2 diabetes.3

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Section: Discussionsupporting

confidence: 68%

The novel NADPH oxidase 4 inhibitor GLX351322 counteracts glucose intolerance in high-fat diet-treated C57BL/6 mice

Anvari

Wikström

Walum

et al. 2015

Free Radical Research

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“…In vitro and other evidence shows that actively insulin-secreting beta cells are more prone to destruction via various mechanisms such as susceptibility to interleukin 1-beta and increased levels of islet antigens [52]. Further experimental animal data have been reviewed and potential mechanisms previously discussed [53].…”

Section: Discussionmentioning

confidence: 99%

Birthweight and the risk of childhood-onset type 1 diabetes: a meta-analysis of observational studies using individual patient data

et al. 2010

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“…Long-term remission of glucose metabolism deterioration, with restoration of beta cell function were reported. [27][28][29][30]. Early detection of patients prone to incipient beta cell failure by monitoring abdominal obesity centralization perhaps using WRSTR in normoglycemic, overweight and obese subjects, followed by intermittent and careful implementation of beta cell rest, might give us new hope in the ongoing battle against type 2 diabetes mellitus.…”

Section: Discussionmentioning

confidence: 99%

Subcutaneous adipose tissue measurements and better metabolic prediction

et al. 2013

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AbstractThe aim of the study was to establish the importance of an additional measurement of subcutaneous adipose tissue thickness (SAT) on a predetermined position on the waistline, and its relation to waist measurements as an improvement of metabolic prediction in equally obese subjects. One hundred and forty two consecutive patients were enrolled in the study: stratified by weight as normal (body mass index — BMI 20–25 kg/m2), overweight (BMI 25–30 kg/m2) and obese (BMI >30 kg/m2); and by fasting glucose level as normoglycemic, impaired fasting glucose (IFG), or with type 2 diabetes mellitus (T2DM). SAT was measured in relaxed expiration, 3 cm left of the umbilicus, with ultrasound. Fasting blood samples for glucose, insulin and HbAlc were taken. Waist circumference was slightly higher in the IFG (112.8 cm) and normoglycemic groups (115.62 cm), compared to T2DM (108.15 cm). The T2DM group had a lower average SAT (2.7 cm) than both the IFG group (3.4 cm, p<0.01) and the normoglycemic group (4.2cm, p=0.001). The homeostatic model of assessment for insulin resistance (HOMA IR) was the lowest in normoglycemic and the highest in IFG group. Waistline radius to SAT ratio provides better insight into the deterioration of glucose metabolism than standard anthropometric markers of abdominal obesity in equally obese patients.

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Effects of beta-cell rest on beta-cell function: a review of clinical and preclinical data

Cited by 95 publications

References 67 publications

The novel NADPH oxidase 4 inhibitor GLX351322 counteracts glucose intolerance in high-fat diet-treated C57BL/6 mice

The novel NADPH oxidase 4 inhibitor GLX351322 counteracts glucose intolerance in high-fat diet-treated C57BL/6 mice

Birthweight and the risk of childhood-onset type 1 diabetes: a meta-analysis of observational studies using individual patient data

Subcutaneous adipose tissue measurements and better metabolic prediction

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