Intermittent food restriction (IFR) is used mainly for weight loss; however, its effects on adipose tissue are not known when alternating with an obesogenic diet. To demonstrate its effects on morphological dynamics of fat deposits, female Wistar rats were distributed into groups: standard control (ST-C), with commercial diet; DIO control (DIO-C), with a diet that induces obesity (DIO) during the first and last 15 d, replaced by a standard diet for thirty intermediate days; standard restricted (ST-R), with standard diet during the first and last 15 d, with six cycles of IFR at 50 % of ST-C; and DIO restricted (DIO-R), in DIO during the first and last 15 d, with six cycles of IFR at 50 % of DIO-C. At 105 d of life, white adipose tissue (WAT) and brown adipose tissue (BAT) deposits were collected, weighed and histology performed. The DIO-R group showed higher total food intake (DIO-R 10 768·0 (SEM 357·52) kJ/g v. DIO-C 8868·6 (SEM 249·25) kJ/g, P < 0·0001), energy efficiency during RAI (DIO-R 2·26 (SEM 0·05) g/kJ v. DIO-C 0·70 (SEM 0·03) g/kJ, P < 0·0001) and WAT (DIO-R 5·65 (SEM 0·30) g/100 g v. DIO-C 4·56 (SEM 0·30) g/100 g) than their respective control. Furthermore, IFR groups presented hypertrophy of WAT and BAT, as well as fibrosis in BAT. Thus, IFR can establish prospective resistance to weight loss by favouring changes in adipose tissue morphology, increased energy intake and efficiency. Finally, the DIO diet before and after IFR aggravates the damages caused by the restriction.

Severe acute malnutrition (SAM) is a major cause of child mortality and morbidity. Children treated for SAM are at risk of refeeding hypophosphataemia (HP). The study was done to find out the incidence and various predictors of moderate/severe HP in SAM among North Indian children. This prospective observational study was conducted from August 2014 to July 2015 in the inpatients’ department of Department of Paediatrics at King George’s Medical University, Lucknow, Uttar Pradesh, North India, a tertiary care teaching hospital. Before inclusion, ethical approval and written informed consent was obtained. Included in the study were sixty-five children aged 6–59 months of age, who were admitted to the hospital with SAM as per the WHO guidelines. SAM was defined as a mid-upper arm circumference <115 mm and/or weight-for-height/length <–3 z-scores of the WHO growth standards and/or have bilateral oedema. Serum P levels were measured on admission and for five consecutive days after starting feed. HP was defined as mild, moderate and severe with a cut-off of 1·19–0·65, 0·65–0·32 and <0·32 mmol/l, respectively. About 60 % children had HP, with 20 % having moderate/severe HP at admission. The proportion of HP increased to 83·1 %, with 38·5 % having moderate/severe HP on day 3 after feeding. It was concluded that HP is a common biochemical abnormality in SAM. Considering its impact on the health of the child, serum P levels should be monitored in patients with SAM who are treated with enteral feeding.

Previous studies suggest that a low-glycaemic index (LGI) diet may improve insulin sensitivity (IS). As IS has been shown to decrease during refeeding, we hypothesised that an LGI- v. high-GI (HGI) diet might have favourable effects during this phase. In a controlled nutritional intervention study, sixteen healthy men (aged 26·8 (sd 4·1) years, BMI 23·0 (sd 1·7) kg/m2) followed 1 week of overfeeding, 3 weeks of energy restriction and of 2 weeks refeeding at ± 50 % energy requirement (50 % carbohydrates, 35 % fat and 15 % protein). During refeeding, subjects were divided into two matched groups receiving either high-fibre LGI or lower-fibre HGI foods (GI 40 v. 74, fibre intake 65 (sd 6) v. 27 (sd 4) g/d). Body weight was equally regained in both groups with refeeding (mean regain 70·5 (sd 28·0) % of loss). IS was improved by energy restriction and decreased with refeeding. The decreases in IS were greater in the HGI than in the LGI group (group × time interactions for insulin, homeostasis model assessment of insulin resistance (HOMAIR), Matsuda IS index (MatsudaISI); all P< 0·05). Mean interstitial glucose profiles during the day were also higher in the HGI group (ΔAUCHGI-LGI of continuous interstitial glucose monitoring: 6·6 mmol/l per 14 h, P= 0·04). At the end of refeeding, parameters of IS did not differ from baseline values in either diet group (adiponectin, insulin, HOMAIR, MatsudaISI, M-value; all P>0·05). In conclusion, nutritional stress imposed by dietary restriction and refeeding reveals a GI/fibre effect in healthy non-obese subjects. LGI foods rich in fibre may improve glucose metabolism during the vulnerable refeeding phase of a weight cycle.

Elucidating the effects of refeeding a high-protein diet after fasting on disease development is of interest in relation to excessive protein ingestion and irregular eating habits in developed countries. The objective of the present study was to address the hepatic effects of refeeding a high-protein diet after fasting. Mice were fasted for 48 h and then refed with a test diet containing 3, 15, 35, 40, 45 or 50 % casein. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and liver immediate-early gene expression levels were sequentially measured for the first 24 h after initiation of refeeding. Refeeding with a 50 % casein diet after 48 h of fasting led to a rapid (within 2–3 h) and abnormal elevation in serum ALT (P = 0·006) and AST (P = 0·001) activities and a marked increase in liver Finkel-Biskis-Jinkins (FBJ) osteosarcoma oncogene (P = 0·007) and nuclear receptor subfamily 4, group A, member 1 (P = 0·002) mRNA levels. In contrast, refeeding of the 3, 15 or 35 % casein diets produced no substantial increases in serum ALT and AST activities in mice. Refeeding of 40, 45 or 50 % casein increased serum ALT and AST activities in proportion to this dietary casein content. In mice refed the 3, 15 or 35, but not 50 %, casein diets, liver heat shock protein 72 transcript levels greatly increased. We conclude from these data that the consumption of a high-protein diet after fasting causes acute hepatocellular injury in healthy animals, and propose that careful attention should be paid to the use of such diets.

The mink is a seasonal breeder with a propensity for seasonal fatness, and it is very responsive to changes in energy supply. The objectives of the present study were first, to validate a multi-species leptin assay for mink (Mustela vison) plasma, and second, to evaluate how plasma leptin and insulin concentrations responded to energy restriction and body-weight loss and refeeding with restoration of body reserves. The study was performed with six very fat yearling females (initial mean body weight 1451 (SD 119) g, i.e. approximately 300 g more than for a female in normal body condition). The animals were fed in restricted amounts (about 35 % metabolizable energy requirement for maintenance) in order to reach a very lean body condition. The target weight of 800 g was reached after about 1 month of restriction. The animals were then refed ad libitum until almost complete weight recovery. Blood samples were taken on days 1, 24, 34 (end of restriction), 44, 55 and 71 (end of experiment) and analysed for plasma concentrations of leptin and insulin. Three females were mated on day 44. Leptin and insulin concentrations mirrored each other and clearly reflected changes in body weight. Significant (P<0·001) Pearson correlation coefficients of 0·75 (leptin–insulin), 0·72 (leptin–body weight) and 0·59 (insulin–body weight) were found. Two of the three females that were mated gave birth to normal litters. It was concluded that the leptin assay yielded acceptable results for animals with body weight:fat content within the range investigated here, and that plasma leptin reflected body fat mass.

The effect of underfeeding and ref eeding on digestion was studied in Bos taurus and Bos indicus cows. Eight nonlactating cows, four B. taurus and four B. indicus (live weight 156 kg and 207 kg respectively) were first given a forage-based diet at a level above energy maintenance requirements for 4 weeks (3·65 and 4·66 kg dry matter (DM) per day respectively for B. taurus and B. indicus). They were then restricted at a low level of intake for 2 months (1·83 and 2·33 kg DM per day respectively for B. taurus and B. indicus) and finally refed at the first level for 2 months. Digestion measurements were made before the underfeeding period, at 3 and 8 weeks of underfeeding and at 3 and 8 weeks ofref eeding. Organic matter apparent digestibility decreased with underfeeding and increased with refeeding (0·637, 0·591, 0·652, 0·692 and 0·669 in B. taurus and 0·674, 0·560, 0·580, 0·698 and 0·692 in B. indicus, respectively 1 week before, 3 and 8 weeks after underfeeding, and 3 and 8 weeks after refeeding). This lower apparent digestibility at low level of intake was not expected either by ruminal particle retention time, which increased when intake decreased, or by measurements ofmicrobial activity: DM degradability measured in situ and ruminal particle size did not vary with level of intake. An effect of the length of underfeeding and refeeding was seen: the apparent digestibility tended to increase after several weeks of undernutrition and was higher after refeeding than before underfeeding. No difference was observed between the two genotypes.

Whole-body fatty acid analysis in rats has previously shown that 50–70% of dietary linoleate and α-linolenate is β-oxidized to CO2 and that this value increases with refeeding after a single episode of fasting. Our hypothesis was that repeated fasting-refeeding or weight-cycling would increase the β-oxidation of linoleate and α-linolenate thereby depleting their whole-body levels. In rats consuming 3% energy as linoleate and 0·15 % energy as α-linolenate during a 16 d balance period, 19% of the linoleate consumed accumulated in weight-cycled rats compared with 34% in the free-fed controls (P < 0.01). Similarly, 11% of the α-linolenate consumed accumulated in the weight-cycled rats compared with 22% in the controls (P < 0.01). Arachidonate and docosahexaenoate also accumulated to lower extents in the weight-cycled rats than in the controls. In contrast, whole-body accumulation of palmitate, stearate and oleate was not different between the weight-cycled group and the controls when measured as a proportion of intake or relative to weight gain. Thus, whole-body depletion of linoleate and α-linolenate did not occurper se but the partitioning of linoleate and α-linolenate was significantly altered by weight-cycling resulting in lower whole-body accumulation and higher apparent oxidation of all polyunsaturates especially linoleate and α-linolenate.