Obese mothers’ offspring develop obesity and metabolic alterations in adulthood. Poor postnatal dietary patterns also contribute to obesity and its comorbidities. We aimed to determine whether in obese mothers’ offspring an adverse postnatal environment, such as high-fat diet (HFD) consumption (second hit) exacerbates body fat accumulation, metabolic alterations and adipocyte size distribution. Female Wistar rats ate chow (C-5 %-fat) or HFD (maternal obesity (MO)-25 %-fat) from weaning until the end of lactation. Male offspring were weaned on either control (C/C and MO/C, maternal diet/offspring diet) or HFD (C/HF and MO/HF) diet. At 110 postnatal days, offspring were killed. Fat depots were excised to estimate adiposity index (AI). Serum glucose, triglyceride, leptin, insulin, insulin resistance index (HOMA-IR), corticosterone and dehydroepiandrosterone (DHEA) were determined. Adipocyte size distribution was evaluated in retroperitoneal fat. Body weight was similar in C/C and MO/C but higher in C/HF and MO/HF. AI, leptin, insulin and HOMA-IR were higher in MO/C and C/HF v. C/C but lower than MO/HF. Glucose increased in MO/HF v. MO/C. C/HF and MO/C had higher triglyceride and corticosterone than C/C, but lower corticosterone than MO/HF. DHEA and the DHEA/corticosterone ratio were lower in C/HF and MO/C v. C/C, but higher than MO/HF. Small adipocyte proportion decreased while large adipocyte proportions increased in MO/C and C/HF v. C/C and exacerbated in MO/HF v. C/HF. Postnatal consumption of a HFD by the offspring of obese mothers exacerbates body fat accumulation as well as the decrease of small and the increase of large adipocytes, which leads to larger metabolic abnormalities.

Although previous studies suggested the protective effect of Zn for type 2 diabetes (T2D), the unitary causal effect remains inconclusive. We investigated the causal effect of Zn as a single intervention on glycaemic control for T2D, using a systematic review of randomised controlled trials and two-sample Mendelian randomisation (MR). Four primary outcomes were identified: fasting blood glucose/fasting glucose, HbA1c, homeostatic model assessment for insulin resistance (HOMA-IR) and serum insulin/fasting insulin level. In the systematic review, four databases were searched until June 2021. Studies, in which participants had T2D and intervention did not comprise another co-supplement, were included. Results were synthesised through the random-effects meta-analysis. In the two-sample MR, we used single-nucleotide polymorphisms (SNP) from MR-base, strongly related to Zn supplements, to infer the relationship causally, but not specified T2D. In the systematic review and meta-analysis, fourteen trials were included with overall 897 participants initially. The Zn supplement led to a significant reduction in the post-trial mean of fasting blood glucose (mean difference (MD): −26·52 mg/dl, 95 % CI (−35·13, −17·91)), HbA1c (MD: −0·52 %, 95 % CI: (−0·90, −0·13)) and HOMA-IR (MD: −1·65, 95 % CI (−2·62, −0·68)), compared to the control group. In the two-sample MR, Zn supplement with two SNP reduced the fasting glucose (inverse-variance weighted coefficient: −2·04 mmol/l, 95 % CI (−3·26, −0·83)). From the two methods, Zn supplementation alone may causally improve glycaemic control among T2D patients. The findings are limited by power from the small number of studies and SNP included in the systematic review and two-sample MR analysis, respectively.

Dietary factors play a role in modulating chronic inflammation and in the development of CVD. We aimed to investigate the association between the dietary inflammatory index (DII) and cardiometabolic risk factors among adolescents. A total of 31 684 Brazilian adolescents (aged 12–17 years) from the Study of Cardiovascular Risks in Adolescents (ERICA) were included. Dietary intake was assessed using a 24-h dietary recall. The energy-adjusted dietary inflammatory index (E-DII) score was calculated based on data for twenty-five available nutrients. The anthropometric profile, blood pressure, lipid profile, glucose, Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) and glycated Hb were measured. Poisson regression models were used to examine the associations between sex-specific quartiles of the E-DII and cardiometabolic risk factors. In the energy-adjusted models, when comparing a high pro-inflammatory diet (quartile 4) with an anti-inflammatory diet (quartile 1), there was a positive association with high HOMA-IR among boys (prevalence ratios (PR)Q4 = 1·37, 95 % CI: 1·04, 1·79); and with high fasting glucose (PRQ4 = 1·96, 95 % CI: 1·02, 3·78), high TAG (PRQ4 = 1·92, 95 % CI: 1·06, 3·46), low HDL-cholesterol (PRQ4 = 1·16, 95 % CI: 1·02, 1·32) and high LDL-cholesterol (PRQ4 = 1·93, 95 % CI: 1·12, 3·33) among girls. Additionally, a moderately pro-inflammatory diet was positively associated with high HOMA-IR (PRQ2 = 1·14, 95 % CI: 1·02, 1·29) among girls and high total cholesterol (PRQ3 = 1·56, 95 % CI: 1·20, 2·01) among boys. In conclusion, this study provides new evidence on the association between inflammatory diets with cardiometabolic risk factors among adolescents.

D-Allulose, also referred to as psicose, is a C3-epimer of D-fructose used as a sugar substitute in low energy products. It can be formed naturally during processing of food and drinks containing sucrose and fructose or is prepared by chemical synthesis or via enzymatic treatment with epimerases from fructose. Estimated intakes via Western style diets including sweetened beverages are below 500 mg per d but, when used as a sugar replacement, intake may reach 10 to 30 g per d depending on the food consumed. Due to its structural similarity with fructose, allulose uses the same transport and distribution pathways. But in contrast to fructose, the human genome does not encode for enzymes that are able to metabolise allulose leading to an almost complete renal excretion of the absorbed dose and near-to-zero energetic yield. However, in vitro studies have shown that certain bacteria such as Klebsiella pneumonia are able to utilise allulose as a substrate. This finding has been a subject of concern, since Klebsiella pneumoniae represents an opportunistic human pathogen. It therefore raised the question of whether a high dietary intake of allulose may cause an undesirable growth advantage for potentially harmful bacteria at mucosal sites such as the intestine or at systemic sites following invasive infection. In this brief review, we discuss the current state of science on these issues and define the research needs to better understand the fate of allulose and its metabolic and microbiological effects when ingested as a sugar substitute.

Personalised nutrition is at its simplest form the delivery of dietary advice at an individual level. Incorporating response to different diets has resulted in the concept of precision nutrition. Harnessing the metabolic phenotype to identify subgroups of individuals that respond differentially to dietary interventions is becoming a reality. More specifically, the classification of individuals in subgroups according to their metabolic profile is defined as metabotyping and this approach has been employed to successfully identify differential response to dietary interventions. Furthermore, the approach has been expanded to develop a framework for the delivery of targeted nutrition. The present review examines the application of the metabotype approach in nutrition research with a focus on developing personalised nutrition. Application of metabotyping in longitudinal studies demonstrates that metabotypes can be associated with cardiometabolic risk factors and diet-related diseases while application in interventions can identify metabotypes with differential responses. In general, there is strong evidence that metabolic phenotyping is a promising strategy to identify groups at risk and to potentially improve health promotion at a population level. Future work should verify if targeted nutrition can change behaviours and have an impact on health outcomes.

Paediatric non-alcoholic fatty liver disease has increased in parallel with childhood obesity. Dietary habits, particularly products rich in sugars, may influence both hepatic fat and insulin resistance (homeostatic model assessment for insulin resistance (HOMA-IR)). The aim of the study was to examine the association of the consumption of foods and food components, dairy desserts and substitutes (DDS), sugar-sweetened beverages (SSB), as well as total and added sugars, with hepatic fat and HOMA-IR. Dietary intake (two non-consecutive 24 h-recalls), hepatic fat (MRI) and HOMA-IR were assessed in 110 overweight/obese children (10·6 (sd 1·1) years old). Linear regression analyses were used to examine the association of dietary intake with hepatic fat and HOMA-IR adjusted for potential confounders (sex, age, energy intake, maternal educational level, total and abdominal adiposity and sugar intake). The results showed that there was a negative association between cereal intake and hepatic fat (β=–0·197, P<0·05). In contrast, both SSB consumption (β=0·217; P=0·028) and sugar in SSB (β=0·210, P=0·035), but not DDS or sugar in DDS or other dietary components, were positively associated with hepatic fat regardless of potential confounders including total sugar intake. In conclusion, cereal intake might decrease hepatic fat, whereas SSB consumption and its sugar content may increase the likelihood of having hepatic steatosis. Although these observations need to be confirmed using experimental evidence, these results suggest that healthy lifestyle intervention programs are needed to improve dietary habits as well as to increase the awareness of the detrimental effects of SSB consumption early in life.