Long-Term Fasting in the Anadromous Arctic Charr Is Associated With Down-Regulation of Metabolic Enzyme Activity and Up-Regulation of Leptin A1 and SOCS Expression in the Liver.

Long-term fasting in the anadromous Arctic charr is associated with down-regulation of metabolic enzyme activity and up-regulation of leptin A1 and SOCS expression in the liver.

J Exp Biol. 2013 May 16;
Jørgensen EH, Martinsen M, Strøm V, Hansen KE, Ravuri CS, Gong N, Jobling M

The life-strategy of the anadromous Arctic charr (Salvelinus alpinus) includes several months of voluntary fasting during overwintering in fresh water leading to emaciation prior to seawater migration in spring. In this study we compared changes in condition, substrate utilization and liver metabolism between captive anadromous charr subjected to food-deprivation during late winter and spring, and conspecifics fed in excess. In March, 9 out of the 10 sampled fed fish had not eaten, indicating that they were a voluntary anorexic state. In June, the fed fish were eating and all had higher body mass (BM), condition factor (CF) and adiposity than in March. In fasted fish there were only small decreases in BM, CF and adiposity between March and May, but all these parameters decreased markedly from May to June. The fasted fish were fat- and glycogen-depleted in June, had suppressed activity of hepatic enzymes involved in lipid metabolism (G6PDH and HOAD) and seemed to rely on protein-derived glucose as a major energy source. This was associated with up-regulated liver gene expression of leptin A1, leptin A2, SOCS1, SOCS2 and SOCS3, and reduced IGF-I expression. In an in vitro study with liver slices it was shown that recombinant rainbow trout leptin stimulated SOCS1 and SOCS3 expression, but not SOCS2, IGF-I or genes of enzymes involved in lipid (G6PDH) and amino acid (AspAT) metabolism. It is concluded that liver leptin interacts with SOCS in a paracrine fashion to suppress lipolytic pathways and depress metabolism when fat stores are depleted. HubMed – eating

Effects of mindful eating training on delay and probability discounting for food and money in obese and healthy-weight individuals.

Behav Res Ther. 2013 Apr 27; 51(7): 399-409
Hendrickson KL, Rasmussen EB

Obese individuals tend to behave more impulsively than healthy weight individuals across a variety of measures, but it is unclear whether this pattern can be altered. The present study examined the effects of a mindful eating behavioral strategy on impulsive and risky choice patterns for hypothetical food and money. In Experiment 1, 304 participants completed computerized delay and probability discounting tasks for food-related and monetary outcomes. High percent body fat (PBF) predicted more impulsive choice for food, but not small-value money, replicating previous work. In Experiment 2, 102 randomly selected participants from Experiment 1 were assigned to participate in a 50-min workshop on mindful eating or to watch an educational video. They then completed the discounting tasks again. Participants who completed the mindful eating session showed more self-controlled and less risk-averse discounting patterns for food compared to baseline; those in the control condition discounted similarly to baseline rates. There were no changes in discounting for money for either group, suggesting stimulus specificity for food for the mindful eating condition. HubMed – eating

Brown adipose tissue thermogenesis precedes food intake in genetically obese Zucker (fa/fa) rats.

Physiol Behav. 2013 May 14;
Kontos A, de Menezes RC, Ootsuka Y, Blessing W

In Sprague Dawley rats, brown adipose tissue (BAT) thermogenesis occurs in an episodic ultradian manner (BAT on-periods) as part of the basic rest-activity cycle (BRAC). Eating occurs approximately 15min after the onset of BAT on-periods. Zucker obese (fa/fa) rats eat larger less frequent meals than control rats. In chronically instrumented conscious unrestrained Zucker obese rats we examined ultradian fluctuations in BAT, body and brain temperature, and the relation between BAT temperature and eating. The interval between BAT temperature peaks for the 12hour dark phase was 121±3 (mean±SE) min for Zucker obese rats and 91±3min for control lean rats (p<0.01). Corresponding values for the light phase were 148±6 and 118±4min (p<0.01). Mean BAT and body temperatures were lower in Zucker obese rats, in comparison with lean controls, during both BAT on-periods and BAT off-periods. Mean brain temperatures were lower during BAT off-periods. Amplitudes of the BRAC-related increases in all 3 temperatures were greater in the Zucker obese rats. Meal onset in Zucker obese rats commenced 15±1min after the onset of a BAT on-period, not significantly different for the delay observed in lean control rats (18±1min, p>0.05). Thus periods between eating are increased in the Zucker obese rats, but the action of leptin, absent in these animals, is not crucial for the timing of eating in relation to increases in BAT and body temperature. Lack of the normal excitatory action of leptin on brain-regulated BAT sympathetic discharge could also contribute to lower BAT thermogenesis in Zucker obese rats. HubMed – eating