Initial successful weight loss is often followed by weight regain after the dietary intervention. Compared with lean people, cellular stress in adipose tissue is increased in obese subjects. However, the relation between cellular stress and the risk for weight regain after weight loss is unclear. Therefore, we determined the expression levels of stress proteins during weight loss and weight maintenance in relation to weight regain. In vivo findings were compared with results from in vitro cultured human Simpson–Golabi–Behmel syndrome (SGBS) adipocytes. In total, eighteen healthy subjects underwent an 8-week diet programme with a 10-month follow-up. Participants were categorised as weight maintainers or weight regainers (WR) depending on their weight changes during the intervention. Abdominal subcutaneous adipose tissue biopsies were obtained before and after the diet and after the follow-up. In vitro differentiated SGBS adipocytes were starved for 96 h with low (0·55 mm) glucose. Levels of stress proteins were determined by Western blotting. WR showed increased expressions of β-actin, calnexin, heat shock protein (HSP) 27, HSP60 and HSP70. Changes of β-actin, HSP27 and HSP70 are linked to HSP60, a proposed key factor in weight regain after weight loss. SGBS adipocytes showed increased levels of β-actin and HSP60 after 96 h of glucose restriction. The increased level of cellular stress proteins in the adipose tissue of WR probably resides in the adipocytes as shown by in vitro experiments. Cellular stress accumulated in adipose tissue during weight loss may be a risk factor for weight regain.

If the depletion of the stratospheric ozone shield continues, the influx of solar UV-B radiation (280–320 nm) will increase in the near future. In photosynthetic organisms there are several targets for the deleterious UV-B radiation, such as proteins, DNA and membranes. Cyanobacteria use three different types of strategies to counteract UV damage: (i) stress avoidance by gliding mechanisms, (ii) stress defence by synthesis of UV-absorbing compounds, antioxidants and extracellular polysaccharides, and (iii) repair mechanisms including DNA repair and resynthesis of UV-sensitive proteins. In the past, most studies concentrated on the physiological aspects of UV tolerance whereas the molecular basis of UV tolerance in cyanobacteria is poorly understood. We will summarize the effects of and responses to UV-B at the physiological and molecular levels and present data on the influence of UV-B irradiation on the proteome of the terrestrial cyanobacterium Nostoc commune. SDS-PAGE and high-resolution two-dimensional gel electrophoresis were used to analyse the influence of UV-B on the proteome of N. commune. The resolution of SDS-PAGE turned out to be far too low to monitor the UV acclimation process. In contrast to the latter technique, two-dimensional electrophoresis showed that the UV-B response is extremely complex, involving the induction and the repression of a large number of proteins.

Well watered (WW) or drought-stressed (DS) saplings of ozone-sensitive and ozone-tolerant (less sensitive) birch (Betula pendula Roth) clones were exposed for 43 d to 0 nl l−1 or 100 nl l−1 ozone. Relative growth rates of leaves, stem, and roots, leaf discolouration, stomatal conductance and induction of genes encoding stress-related proteins PR-10, PAL and a LEA-group protein BP8 were determined. In general, both ozone and drought stress, singly and in combination, increased transcript levels of PR-10 in both clones. This was related to lower induction of PAL (except in older leaves of the tolerant clone), and increased proportions of visibly injured and yellowed leaves in ozone-exposed plants. The clones differed in their stomatal conductance and growth responses. In the less sensitive clone 2, ozone did not affect growth rates, but high stomatal conductance was observed in WW ozone-exposed plants. The more sensitive clone 5 showed, on the contrary, reduced growth rates and low stomatal conductance in WW ozone plants. Interestingly, clone 2 was sensitive to drought stress alone, whereas clone 5 was highly sensitive to ozone and drought stress experienced together. The results show that appearance of visible injuries (necrotic flecks) and enhanced yellowing of leaves coincided with the induction of genes for stress proteins PR-10 and PAL. The short-term growth responses, however, seemed to be separate processes. Additionally, stomatal conductance was related to leaf injuries and growth rates in a complicated manner, emphasizing the complex nature of ozone sensitivity/tolerance mechanisms in birch.