Impact of Whole, Fresh Fruit Consumption on Energy Intake and Adiposity: A Systematic Review

Background: The energy content of whole, fresh fruit derives primarily from simple sugars, which are currently under heightened scrutiny for their potential contribution to obesity and chronic disease risk. Yet fruit also has a relatively low energy density, moderate palatability/reward value, and high fiber content, which together may limit energy intake. Although reasoned arguments can be made that fruit is fattening or slimming, the question is best resolved empirically.Methods: Methods were preregistered with PROSPERO (CRD42018111830). The primary outcome is the impact of whole, fresh fruit consumption on measures of adiposity including body weight in randomized controlled trials (RCTs). Secondary outcomes are the impact of whole, fresh fruit consumption on energy intake in RCTs, and the association between whole, fresh fruit consumption and changes in measures of adiposity in prospective observational studies. CENTRAL and PubMed databases were searched through October 2018. Cochrane risk of bias tool was used to assess risk of bias in RCTs, and the GRADE method was used to judge and convey the certainty of conclusions. Reporting follows PRISMA guidelines.Results: RCTs, and particularly those of higher quality, suggest that increasing whole, fresh fruit consumption promotes weight maintenance or modest weight loss over periods of 3–24 weeks (moderate certainty), with limited evidence suggesting that a high intake of fruit favors weight loss among people with overweight or obesity. Consistent with this, single-meal RCTs suggest that consuming whole, fresh fruit tends to decrease energy intake, particularly when consumed prior to a meal or when displacing more energy-dense foods (moderate certainty). Prospective observational studies suggest that habitually higher fruit intake is not associated with weight change, or is associated with modest protection against weight gain, over five or more years.Conclusions: Current evidence suggests that whole, fresh fruit consumption is unlikely to contribute to excess energy intake and adiposity, but rather has little effect on these outcomes or constrains them modestly. Single-meal RCTs, RCTs lasting 3–24 weeks, and long-term observational studies are relatively consistent in supporting this conclusion. Whole, fresh fruit probably does not contribute to obesity and may have a place in the prevention and management of excess adiposity

The SAGA Histone Deubiquitinase Module Controls Yeast Replicative Lifespan via Sir2 Interaction

We have analyzed the yeast replicative lifespan of a large number of open reading frame (ORF) deletions. Here, we report that strains lacking genes SGF73, SGF11, and UBP8 encoding SAGA/SLIK complex histone deubiquitinase module (DUBm) components are exceptionally long lived. Strains lacking other SAGA/SALSA components, including the acetyltransferase encoded by GCN5, are not long lived; however, these genes are required for the lifespan extension observed in DUBm deletions. Moreover, the SIR2-encoded histone deacetylase is required, and we document both a genetic and physical interaction between DUBm and Sir2. A series of studies assessing Sir2-dependent functions lead us to propose that DUBm strains are exceptionally long lived because they promote multiple prolongevity events, including reduced rDNA recombination and altered silencing of telomere-proximal genes. Given that ataxin-7, the human Sgf73 ortholog, causes the neurodegenerative disease spinocerebellar ataxia type 7, our findings indicate that the genetic and epigenetic interactions between DUBm and SIR2 will be relevant to neurodegeneration and aging

Obesity is associated with hypothalamic injury in rodents and humans

Rodent models of obesity induced by consuming high-fat diet (HFD) are characterized by inflammation both in peripheral tissues and in hypothalamic areas critical for energy homeostasis. Here we report that unlike inflammation in peripheral tissues, which develops as a consequence of obesity, hypothalamic inflammatory signaling was evident in both rats and mice within 1 to 3 days of HFD onset, prior to substantial weight gain. Furthermore, both reactive gliosis and markers suggestive of neuron injury were evident in the hypothalamic arcuate nucleus of rats and mice within the first week of HFD feeding. Although these responses temporarily subsided, suggesting that neuroprotective mechanisms may initially limit the damage, with continued HFD feeding, inflammation and gliosis returned permanently to the mediobasal hypothalamus. Consistent with these data in rodents, we found evidence of increased gliosis in the mediobasal hypothalamus of obese humans, as assessed by MRI. These findings collectively suggest that, in both humans and rodent models, obesity is associated with neuronal injury in a brain area crucial for body weight control