The canine golden retriever muscular dystrophy (GRMD) model is the best animal model for studying Duchenne muscular dystrophy in humans. Considering the importance of glucose metabolism in the muscles, the existence of metabolic and endocrine alterations in a wide range of muscular dystrophies, and the pre-existing relationship between blood insulin concentration and muscular atrophy, the present study aimed to evaluate the postprandial glucose and insulin response in GRMD dogs. A total of eighteen golden retriever dogs were randomly distributed into three experimental groups: healthy/control (G1), female GRMD carriers (G2), and male dogs affected by GRMD (G3). Higher plasma resting glucose levels (P = 0·0047) were seen in G2 and G3 compared with G1, as was the case for minimum (P = <0·0001), mean (P = 0·0002) and maximum (P = 0·0359) glucose values for G3 compared with G1. Fructosamine concentrations were in accordance with reference values found in the literature for dogs. Insulin levels were lower in G3 compared with G1 (P = 0·0065); however, there was no evidence of insulin resistance according to the homeostasis model assessment index values obtained. As for the evaluation of postprandial responses, fluctuations of glucose (P = 0·0007) and insulin (P = 0·0149) were observed in G1 and G2, while in G3 the values remained constant. The results allowed us to identify metabolic changes related to carbohydrate metabolism in GRMD dogs, highlighting the importance of adequate food management for these animals.

Obesity is associated with low-grade inflammation, triggered in adipose tissue, which may occur due to an excess of SFA from the diet that can be recognised by Toll-like receptor-4. This condition is involved in the development of components of the metabolic syndrome associated with obesity, especially insulin resistance. The aim of the study was to evaluate the manifestation of the metabolic syndrome and adipose tissue inflammation as a function of the period of time in which rats were submitted to a high-sugar/fat diet (HSF). Male Wistar rats were divided into six groups to receive the control diet (C) or the HSF for 6, 12 or 24 weeks. HSF increased the adiposity index in all HSF groups compared with the C group. HSF was associated with higher plasma TAG, glucose, insulin and leptin levels. Homeostasis model assessment increased in HSF compared with C rats at 24 weeks. Both TNF-α and IL-6 were elevated in the epididymal adipose tissue of HSF rats at 24 weeks compared with HSF at 6 weeks and C at 24 weeks. Only the HSF group at 24 weeks showed increased expression of both Toll-like receptor-4 and NF-κB. More inflammatory cells were found in the HSF group at 24 weeks. We can conclude that the metabolic syndrome occurs independently of the inflammatory response in adipose tissue and that inflammation is associated with hypertrophy of adipocytes, which varies according to duration of exposure to the HSF.

A population-based cross-sectional study was carried out in the northern neighbourhoods of Ouagadougou (Burkina Faso), to examine the relationship of nutritional deficiencies and cardiometabolic risk factors (CMRF) with lifestyle in adults. We randomly selected 330 households stratified by income tertile. In each income stratum, 110 individuals aged 25–60 years and having lived in Ouagadougou for at least 6 months were randomly selected. We performed anthropometric, dietary intake and physical activity measurements, and blood sample collection. Cluster analysis of dietary intake identified two dietary patterns: ‘urban’ (29 % of subjects) and ‘traditional’ (71 %). The ‘urban’ cluster exhibited a higher intake of fat and sugar, whereas a higher intake of plant protein, complex carbohydrate and fibre was observed in the ‘traditional’ pattern. Female sex, low income and lack of education were associated with the ‘traditional’ cluster, as well as Fe and vitamin A deficiency. CMRF prevalence (abdominal obesity, hypertension, hyperglycaemia, dyslipidaemia) was similar in both clusters. Subjects in the ‘traditional’ cluster spent more time in physical activity and had less sedentary time than those in the ‘urban’ cluster. ‘Traditional’ dietary pattern, low income, female sex and sedentary time were significant contributing factors to the double burden of malnutrition. The rapid nutrition transition is reflected in this co-occurrence of CMRF and nutritional deficiencies. This stresses the need for prevention strategies addressing both ends of the nutrition spectrum.

SCFA provide energy to the host and influence lipid and glucose metabolism, suggesting that they may have an impact on the occurrence of metabolic risk factors. The aim of the present study was to determine the concentration of SCFA in faeces of lean and obese individuals and to analyse whether associations between faecal SCFA and metabolic syndrome parameters are present. Lean (n 20) and obese (n 20) women of similar age (28·5 (sd 7·6) v. 30·7 (sd 6·5) years, P= 0·33) participated in the study. Anthropometric measurements, body composition, blood pressure and biochemical parameters were assessed. SCFA were extracted from faeces and quantified by GC. Blood pressure and blood glucose, although within the normal limits, were higher in the obese group compared to lean subjects (P< 0·05). Lower HDL concentration and higher insulin and homeostasis model assessment (HOMA) index were observed in the obese than in the lean group (P< 0·05). The median values of SCFA (% w/w) from the lean and obese groups were butyric (0·021 v. 0·044, P= 0·024), propionic (0·021 v. 0·051, P= 0·007) and acetic (0·03 v. 0·061, P= 0·01). SCFA correlated positively with metabolic syndrome risk factors such as adiposity, waist circumference and HOMA index (P< 0·05), and inversely with HDL (P< 0·05). Our results suggest that the higher faecal concentration of SCFA is associated with metabolic risk factors and thus may influence metabolic homeostasis.

In the Western world, a trend towards increased consumption of carbonated soft drinks combined with a decreasing intake of milk is observed. This may affect circulating insulin-like growth factor I (IGF-I) and fasting insulin, as seen in pre-pubertal children. The present study was designed to reflect the trend of replacing milk with carbonated beverages in young men and to study the effects of this replacement on IGF-I, IGF-binding protein 3 (IGFBP-3), IGF-I:IGFBP-3 and glucose–insulin metabolism. A randomised, controlled crossover intervention study, in which eleven men aged 22–29 years were given a low-Ca diet in two 10 d periods with 10 d washout in between. In one period, they drank 2·5 litres of Coca Cola® per day and the other period 2·5 litres of semi-skimmed milk. Serum IGF-I, IGFBP-3 (RIA), insulin (fluoro immunoassay) and glucose (Cobas) were determined at baseline and end point of each intervention period. Insulin resistance and β-cell function were calculated with the homeostasis model assessment. A decrease in serum IGF-I was observed in the cola period compared with the milk period (P < 0·05). No effects of treatment were observed on IGFBP-3, IGF-I:IGFBP-3, insulin, glucose, insulin resistance or β-cell function. The present study demonstrates that high intake of cola over a 10 d period decreases total IGF-I compared with a high intake of milk, with no effect on glucose–insulin metabolism in adult men. It is unknown whether this is a transient phenomenon or whether it has long-term consequences.

The purpose of the present study was to evaluate the effect of Ramadan fasting on insulin sensitivity in subjects with the metabolic syndrome. Males (n 55; age 34·1 (sd 8·9) years) with the metabolic syndrome were studied. Blood pressure, waist circumference, body weight, HDL-cholesterol (HDL-C), TAG, fasting plasma glucose (FPG), fasting blood insulin and insulin resistance indices (quantitative insulin sensitivity check index (QUICKI), homeostasis model assessment of insulin resistance (HOMA-IR) and reciprocal index of HOMA-IR (1/HOMA-IR)) were evaluated before and after 30 d of Ramadan fasting (two meals at 12 h intervals). The dietary intake was estimated by 24 h recall before and after fasting. The total daily energy intake was decreased by 234·6 (sd 88·2) kJ/d in the fasting period (P = 0·005). 1/HOMA-IR, QUICKI and HDL-C were significantly increased (P = 0·005, P = 0·001 and P = 0·004) and FPG significantly decreased (P < 0·005) after fasting. Simple linear regression analysis demonstrated that HOMA-IR, 1/HOMA-IR and QUICKI were related to waist circumference after intervention (r 0·458, P < 0·001; r − 0·396, P < 0·05; r − 0·342, P < 0·05). In conclusion, the present study showed that the combined change in the number and timing of meals and portioning of the entire intake into only two meals per d may increase insulin sensitivity in subjects with the metabolic syndrome even when the decrease in energy consumption is minimal.

Protein–energy malnutrition promotes adaptive hormonal changes that result in stunting. A previous study showed that stunted children had increased insulin sensitivity and diminished pancreatic β-cell function. The objectives of the present study were to analyse the glucose, insulin, homeostasis model assessment of insulin sensitivity (HOMA-S) and homeostasis model assessment of pancreatic β-cell function (HOMA-B) levels after nutritional recovery. The recovered group (n 62) consisted of malnourished children after treatment at a nutrition rehabilitation centre. At the beginning of treatment their age was 2·41 (sd 1·28) and 2·31 (sd 1·08) years, weight-for-age Z score − 2·09 (sd 0·94) and − 2·05 (sd 0·55) and height-for-age Z score − 1·85 (sd 1·11) and − 1·56 (sd 0·90), for boys and girls respectively. The control group consisted of well-nourished children without treatment (n 26). After treatment, boys of the recovered group gained 1·29 (sd 1·06) Z scores of height-for-age and 1·14 (sd 0·99) Z scores of weight-for-age, and girls, 1·12 (sd 0·91) and 1·21 (sd 0·74) Z scores respectively. No differences were found between control and recovered groups in insulin levels for boys (P = 0·704) and girls (P = 0·408), HOMA-B for boys (P = 0·451) and girls (P = 0·330), and HOMA-S (P = 0·765) for boys and girls (P = 0·456) respectively. The present study shows that the changes observed previously in glucose metabolism and insulin were reverted in children who received adequate treatment at nutritional rehabilitation centres and showed linear catch-up.