Lifestyle interventions for weight loss in adults with severe obesity: a systematic review.

Severe obesity is an increasingly prevalent condition and is often associated with long-term comorbidities, reduced survival and higher healthcare costs. Non-surgical methods avoid the side effects, complications and costs of surgery, but it is unclear which non-surgical method is most effective. The objective of this article was to systematically review the effectiveness of lifestyle interventions compared to standard or minimal care for weight loss in adults with severe obesity. MEDLINE, EMBASE, CENTRAL, databases of on-going studies, reference lists of any relevant systematic reviews and the Cochrane Library database were searched from inception to February 2016 for relevant randomized controlled trials (RCTs). Inclusion criteria were participants with severe obesity (body mass index [BMI] > 40 kg/m2 or BMI > 35 kg/m2 with comorbidity) and interventions with a minimal duration of 12 weeks that were multi-component combinations of diet, exercise and behavioural therapy. Risk of bias was evaluated using the Cochrane risk of bias criteria. Meta-analysis was not possible because of methodological heterogeneity. Seventeen RCTs met the inclusion criteria. Weight change in kilograms of participants from baseline to follow-up was reported for 14 studies. Participants receiving the lifestyle intervention had a greater decrease in weight than participants in the control group for all studies (1.0-11.5 kg). Lifestyle interventions varied greatly between the studies. Overall lifestyle interventions with combined diet and exercise components achieved the greatest weight loss. Lifestyle interventions for weight loss in adults with severe obesity were found to result in increased weight loss when compared to minimal or standard care, especially those with combined diet and exercise components.

Identification of an inward rectifier potassium channel gene expressed in mouse cortical astrocytes.

These experiments identify an inward rectifier K+ (Kir) channel expressed in mouse cortical and white matter astrocytes at the molecular level. Messenger RNA for one of the known Kir channel genes, Kir4.1, is present at much higher levels in cortical astrocytes in primary culture than the other known Kir family members. In culture, the level of Kir4.1 mRNA is lower in proliferating cells and in cells cultured for 16 h under hypoxic conditions, compared to confluent cells. Partial differentiation of the astrocytes with dibutyryl cAMP or by coculture with neurons has no effect on the Kir4.1 mRNA level. In situ hybridization experiments show that Kir4.1 mRNA is broadly distributed in the adult brain, including the neocortex, the stratum pyrimadale of the hippocampus, and the piriform cortex. Immunostaining confirms that the Kir4.1 protein is expressed by cultured astrocytes and also by cocultured cortical neurons. Astrocytes and neurons display a patchy pattern of immunostaining, raising the possibility that the channels sort themselves in clusters in the plasma membrane. Stellate cells in the neocortex and white matter are immunoreactive for Kir4.1, and double immunofluorescence experiments show colocalization of Kir4.1 and glial acidic fibrillary protein (GFAP) on stellate cells in the white matter. The cloned mouse Kir4.1 cDNA, when expressed heterologously in HEK cells, gives rise to inactivating Kir channels similar to those recorded from cultured astrocytes. These results indicate that the Kir4.1 gene product forms a Kir channel, or is a subunit of the channel, in mouse cortical astrocytes both in culture and in vivo.

Somatostatin mRNA and molecular forms during development of the rat retina.

The developmental control of rat retinal somatostatin (SS) expression was determined by Northern blot hybridization. The amount of SS transcript is higher than adult levels at embryonic day 16 and declines during late prenatal development. This pattern parallels the developmental expression of somatostatin immunoreactivity. The expression of somatostatin-immunoreactive peptide products using gel filtration chromatography was determined over the same period. Three molecular weight forms occur during development: a high m.wt. product and two smaller peptides which migrate with somatostatin-28 (SS28) and somatostatin-14 (SS14). SS14 is the peptide that predominates at all developmental time points, and is the only form detectable in the adult retina. The transient prenatal increase of somatostatin message and peptide suggests a role for this peptide in the developing retina.

Mitochondrial metabolism following traumatic brain injury in rats.

Although a number of studies of traumatic brain injury have implicated mitochondrial dysfunction as a cause of altered posttraumatic energy metabolism, no studies to date have isolated mitochondria and measured their respiratory capacity following trauma. The present study sought to determine whether mitochondrial capacity for oxidative phosphorylation is adversely affected by fluid-percussion-induced traumatic brain injury in rats. Prior to brain injury, the mitochondrial respiratory control ratio was 4.3 +/- 0.2 and the ratio of nmoles of ADP phosphorylated per natom oxygen consumed (ADP/O ratio) was 2.66 +/- 0.09. After injury (2.8 atm; t = 4 h), there were slight but not significant alterations in ADP/O ratio (2.41 +/- 0.07) and state 3 respiratory rate (ADP stimulated); however, there were no changes in the respiratory control ratio. These data suggest that traumatic brain injury, unlike ischemia, does not cause uncoupling of ATP synthesis from respiration, and that brain mitochondria are quite resistant to trauma-induced injury.

Alterations in regional concentrations of endogenous opioids following traumatic brain injury in the cat.

Delayed injury following trauma to the central nervous system (CNS) may be due to the release or activation of endogenous factors. Endogenous opioid peptides have been proposed as one such class of injury factors, based on pharmacological studies demonstrating a therapeutic effect of naloxone and other opiate receptor antagonists following CNS injury. However, changes in brain opioid concentrations following injury have not been evaluated. In the present study, we measured regional alterations in dynorphin (ir-Dyn), leucine-enkephalin (ir-Enk) and beta-endorphin immunoreactivity (ir-End) following low- (1.0-2.0 atmospheres (atm)) or high- (3.0-4.0 atm) level fluid-percussion brain injury in the cat. A significant decrease in ir-End was observed in the hypothalamus at 2 h following high- but not low-level injury. No changes were observed in tissue ir-Enk following either level of injury. Severe brain trauma but not low-level injury caused a significant increase in ir-Dyn in the striatum, frontal cortex, parietal cortex, pons and medulla. In the anterior pituitary, a significant increase in ir-End and a significant decrease in ir-Dyn was observed at 2 h following both levels of injury. Pathological damage to brain tissue after injury was most pronounced in those regions showing significant increases in ir-Dyn but not other opioids. In the medulla, the increase in ir-Dyn but not ir-End or ir-Enk was also significantly correlated with a fall in systemic mean arterial pressure (MAP) at 2 h following high- but not low-level injury.(ABSTRACT TRUNCATED AT 250 WORDS)