Energy restriction (ER) has anti-ageing effects and probably protects from a range of chronic diseases including cancer, diabetes and chronic kidney disease (CKD). Specifically, ER has a positive impact on experimental kidney ageing, CKD (diabetic nephropathy, polycystic kidney disease) and acute kidney injury (nephrotoxic, ischaemia–reperfusion injury) through such mechanisms as increased autophagy, mitochondrial biogenesis and DNA repair, and decreased inflammation and oxidative stress. Key molecules contributing to ER-mediated kidney protection include adenosine monophosphate-activated protein kinase, sirtuin-1 and PPAR-γ coactivator 1α. However, CKD is a complex condition, and ER may potentially worsen CKD complications such as protein–energy wasting, bone–mineral disorders and impaired wound healing. ER mimetics are drugs, such as metformin and Na–glucose co-transporter-2 which mimic the action of ER. This review aims to provide comprehensive data regarding the effect of ER on CKD progression and outcomes.

Previous nutritional studies have shown that insulin regulation is different between DT and A strains of gibel carp. As leptin plays a pivotal role in the effects of insulin, we hypothesised that leptin regulation of glucose and lipid metabolism would differ between the two strains. To test our hypothesis, recombinant human leptin was injected into two strains. The results showed that leptin activated the phosphatidylinositol 3-kinase (PI3K)–protein kinase B (AKT), AMP-activated protein kinase–acetyl coenzyme A carboxylase and Janus kinase 2 (JAK2)–signal transducer and activator of transcription (STAT) signalling pathways in both strains. Hypoglycaemia induced by leptin might be due to higher glucose uptake by the liver and muscles together with enhanced glycolytic potential and reduced gluconeogenic potential. Decreased lipogenesis and up-regulated fatty acid oxidation were induced by leptin. In terms of genotype, the PI3K–AKT signalling pathway was more strongly activated by leptin in the muscle tissue of the A strain, as reflected by the heightened phosphorylation of AKT. Furthermore, glycogen content, glycolytic enzyme activity and gluconeogenic capability were higher in the A strain than the DT strain. Strain A had higher levels of fatty acid synthesis and lipolytic capacity in the liver than the DT strain, but the opposite was true in white muscle. Regarding leptin–genotype interactions, the DT strain displayed stronger regulation of glucose metabolism in the liver by leptin as compared with the A strain. Moreover, a more active JAK2–STAT signalling pathway accompanied by enhanced inhibition of fatty acid synthesis by leptin was observed in the DT strain. Overall, the regulation of glucose and lipid metabolism by leptin differed between the two strains, as expected.

This study reports the validity of body fat percentage (BF%) estimates from several commonly employed techniques as compared with a five-component (5C) model criterion. Healthy adults (n 170) were assessed by dual-energy X-ray absorptiometry (DXA), air displacement plethysmography (ADP), multiple bioimpedance techniques and optical scanning. Output was also used to produce a criterion 5C model, multiple variants of three- and four-component models (3C; 4C) and anthropometry-based BF% estimates. Linear regression, Bland–Altman analysis and equivalence testing were performed alongside evaluation of the constant error (CE), total error (TE), se of the estimate (SEE) and coefficient of determination (R2). The major findings were (1) differences between 5C, 4C and 3C models utilising the same body volume (BV) and total body water (TBW) estimates are negligible (CE ≤ 0·2 %; SEE < 0·5 %; TE ≤ 0·5 %; R2 1·00; 95 % limits of agreement (LOA) ≤ 0·9 %); (2) moderate errors from alternate TBW or BV estimates in multi-component models were observed (CE ≤ 1·3 %; SEE ≤ 2·1 %; TE ≤ 2·2 %; R2 ≥ 0·95; 95 % LOA ≤ 4·2 %); (3) small differences between alternate DXA (i.e. tissue v. region) and ADP (i.e. Siri v. Brozek equations) estimates were observed, and both techniques generally performed well (CE < 3·0 %; SEE ≤ 2·3 %; TE ≤ 3·6 %; R2 ≥ 0·88; 95 % LOA ≤ 4·8 %); (4) bioimpedance technologies performed well but exhibited larger individual-level errors (CE < 1·0 %; SEE ≤ 3·1 %; TE ≤ 3·3 %; R2 ≥ 0·94; 95 % LOA ≤ 6·2 %) and (5) anthropometric equations generally performed poorly (CE 0·6– 5·7 %; SEE ≤ 5·1 %; TE ≤ 7·4 %; R2 ≥ 0·67; 95 % LOA ≤ 10·6 %). Collectively, the data presented in this manuscript can aid researchers and clinicians in selecting an appropriate body composition assessment method and understanding the associated errors when compared with a reference multi-component model.

The effects of resistant starch on glycaemic control are controversial. In this study, a systematic review and meta-analysis of results from nineteen randomised controlled trials (RCT) was performed to illustrate the effects of resistant starch on glycaemic control. A literature search was conducted on PubMed, Scopus and Cochrane electronic databases for related publications from inception to 6 April 2020. Key inclusion criteria were: RCT; resistant starch as intervention substances and reporting glucose- and insulin-related endpoints. Exclusion criteria were: using type I resistant starch or a mixture of resistant starch and other functional food ingredients as intervention; using substances other than digestible starch as controls. The effect of resistant starch on fasting plasma glucose was significant (effect size (ES) –0·09 (95 % CI –0·13, −0·04) mmol/l, P = 0·001) compared with digestible starch. Subgroup analyses revealed that the ES was larger when the dosage of resistant starch was more than 28 g/d (ES –0·16 (95 % CI –0·24, –0·08) mmol/l, P < 0·001) or the intervention period was more than 8 weeks (ES –0·12 (95 % CI –0·18, –0·06) mmol/l, P < 0·001). The effect on homoeostatic model assessment (HOMA)-insulin resistance (IR) was significant (ES –0·33 (95 % CI –0·51, –0·14), P = 0·001). However, the effects on other insulin-related endpoints were not significant, including fasting plasma insulin, four endpoints from the frequently sampled intravenous glucose tolerance test (insulin sensitivity index, acute insulin response, disposition index and glucose effectiveness) and HOMA-β. The current study indicated moderate effects of resistant starch on improving glycaemic control.

The aim of this study was to assess the ability of the FFQ to describe reliable and valid dietary pattern (DP) scores. In a total of 134 participants of the European Prospective Investigation into Cancer and Nutrition-Potsdam study aged 35–67 years, the FFQ was applied twice (baseline and after 1 year) to assess its reliability. Between November 1995 and March 1997, twelve 24-h dietary recalls (24HDR) as reference instrument were applied to assess the validity of the FFQ. Exploratory DP were derived by principal component analyses. Investigated predefined DP were the Alternative Healthy Eating Index (AHEI) and two Mediterranean diet indices. From dietary data of each FFQ, two exploratory DP were retained, but differed in highly loading food groups, resulting in moderate correlations (r 0·45–0·58). The predefined indices showed higher correlations between the FFQ (r(AHEI) 0·62, r(Mediterranean Diet Pyramid Index (MedPyr)) 0·62 and r(traditional Mediterranean Diet Score (tMDS)) 0·51). From 24HDR dietary data, one exploratory DP retained differed in composition to the first FFQ-based DP, but showed similarities to the second DP, reflected by a good correlation (r 0·70). The predefined DP correlated moderately (r 0·40–0·60). To conclude, long-term analyses on exploratory DP should be interpreted with caution, due to only moderate reliability. The validity differed extensively for the two exploratory DP. The investigated predefined DP showed a better reliability and a moderate validity, comparable to other studies. Within the two Mediterranean diet indices, the MedPyr performed better than the tMDs in this middle-aged, semi-urban German study population.

This cross-sectional study aimed to examine the associations between dietary fibre (DF) intake and depressive symptoms in a general adult population in Tianjin, China. A total of 24 306 participants (mean age 41 years; range 18–91 years) were enrolled. DF intake was assessed using a validated self-administered FFQ. Depressive symptoms were assessed using the Self-Rating Depression Scale. Associations between DF intake and depressive symptoms were estimated using logistic regression analysis. Socio-demographic, behavioural, health status and dietary factors were adjusted. In men, compared with participants in the lowest quartiles for total, soluble, vegetable and soya DF, OR for depressive symptoms in the highest were 0·83 (95 % CI 0·69, 0·99), 0·74 (95 % CI 0·63, 0·87), 0·79 (95 % CI 0·65, 0·96) and 0·69 (95 % CI 0·60, 0·81), respectively. In women, compared with participants in the lowest quartiles for vegetable and soya DF, the OR for depressive symptoms in the highest were 0·77 (95 % CI 0·64, 0·93) and 0·82 (95 % CI 0·70, 0·95), respectively. No association was found between total or soluble DF intake and depressive symptoms in women. No association was found between insoluble, cereal, fruit or tuber DF intake and depressive symptoms in men and women. Linear associations between DF intake and depressive symptoms were only detected for soya DF (men, β = –0·148, P < 0·0001; women, β = –0·069, P = 0·04). Results suggest that intake of soluble, vegetable and soya DF was inversely associated with depressive symptoms. These results should be confirmed through prospective and interventional studies.

The role of socio-economic status (SES) on the misreporting of food and energy intakes is not well understood with disagreement in the literature. The aim of this study was to examine the associations between low energy reporting, dietary quality and SES in a representative sample of adults. Dietary data were collected using 2 d of 24-h recalls for 6114 adults aged 19 years and over, participating in the Australian National Nutrition and Physical Activity Survey 2011–2012. Low energy reporters (LER) and plausible reporters (PR) were identified. Discretionary food intake was used as a proxy indicator of diet quality. SES was determined using area-level SES and educational attainment. Regression analysis was applied to examine the effects of LER and SES on diet quality, adjusting for potential confounders. LER was more common in populations of lower SES than higher SES (area-level OR 1·46 (95 % CI 1·06, 2·00); education OR 1·64 (95 % CI 1·28, 2·09). LER and SES were independently associated with diet quality, with LER reporting lower percentage energy from discretionary foods compared with PR (27·4 v. 34·2, P < 0·001), and those of lower area-level SES and education reporting lower diet quality compared with those of higher SES (33·7 v. 31·2, P < 0·001; and 33·5 v. 29·6, P < 0·001, respectively). No interaction effect was found between LER and SES, indicating percentage energy in discretionary foods was not differentially misreported across the SES areas (0·3078) or education (P = 0·7078). In conclusion, LER and higher SES were associated with better diet quality.

Accurate and timely data are essential for identifying populations at risk for undernutrition due to poor-quality diets, for implementing appropriate interventions and for evaluating change. Life-logging wearable cameras (LLWC) have been used to prospectively capture food/beverage consumed by adults in high-income countries. This study aimed to evaluate the concurrent criterion validity, for assessing maternal and child dietary diversity scores (DDS), of a LLWC-based image-assisted recall (IAR) and 24-h recall (24HR). Direct observation was the criterion method. Food/beverage consumption of rural Eastern Ugandan mothers and their 12–23-month-old child (n 211) was assessed, for the same day for each method, and the IAR and 24HR DDS were compared with the weighed food record DDS using the Bland–Altman limits of agreement (LOA) method of analysis and Cohen’s κ. The relative bias was low for the 24HR (–0·1801 for mothers; –0·1358 for children) and the IAR (0·1227 for mothers; 0·1104 for children), but the LOA were wide (–1·6615 to 1·3012 and –1·6883 to 1·4167 for mothers and children via 24HR, respectively; –2·1322 to 1·8868 and –1·7130 to 1·4921 for mothers and children via IAR, respectively). Cohen’s κ, for DDS via 24HR and IAR, was 0·68 and 0·59, respectively, for mothers, and 0·60 and 0·59, respectively, for children. Both the 24HR and IAR provide an accurate estimate of median dietary diversity, for mothers and their young child, but non-differential measurement error would attenuate associations between DDS and outcomes, thereby under-estimating the true associations between DDS – where estimated via 24HR or IAR – and outcomes measured.

We previously reported that dietary vitamin E deficiency increased anxiety-like behaviour in rats exposed to social isolation. Here, we performed a detailed investigation of this phenomenon and its underlying mechanism. First, we fed Wistar rats with a vitamin E-free diet for 3 d, 1 week or 2 weeks and found an increase in anxiety-like behaviour after 1 and 2 weeks of vitamin E deficiency based on behavioural indicators. Next, we examined the effect of a control diet (150 mg all-racemic α-tocopheryl acetate/kg) on anxiety-like behaviours in rats that received a 4-week vitamin E-free diet. We found that increased anxiety-like behaviour was reversed to control levels after refeeding vitamin E for 7 d but not for 1 or 3 d. Further, anxiety-like behaviour increased or decreased gradually based on the amount of vitamin E intake; however, it had a quicker progression than physical symptoms of vitamin E deficiency. Moreover, rats fed with excess vitamin E (500 mg all-racemic α-tocopherol/kg diet) showed less anxiety-like behaviour than control rats, indicating that vitamin E supplementation is effective for preventing anxiety increase under social isolation stress. Since plasma corticosterone levels were higher in vitamin E-deficient rats, we investigated the effect of adrenalectomy on anxiety-like behaviour and found that adrenal hormones played an essential role in the increased anxiety-like behaviour induced by vitamin E deficiency. In conclusion, increased anxiety-like behaviour is a symptom that emerges earlier than physical vitamin E deficiency and is caused by adrenal hormone-dependent mechanisms.