Activity

The current analysis used functional magnetic resonance imaging (fMRI) to explore a model of energy regulation postulating that the hippocampus integrates interoceptive signals and environmental stimuli to suppress responding to food cues. It was hypothesized that hippocampal activity would increase in response to food cues under postnutritive relative to fasted conditions, given the role of the hippocampus in integrating postnutritive signals with food cues, and that obesity, added sugar intake, or a combination of these factors would alter this response.

Data were analyzed on 65 participants (29 males). Participants consumed drinks containing 75 g of glucose or water and underwent an fMRI-based food-cue task. Blood-oxygen-level-dependent (BOLD) fMRI was used to examine hippocampal responses to food and nonfood cues.

In lean participants, the hippocampal BOLD signal was higher following glucose compared with water, but participants with obesity showed the opposite pattern. BMI interacted with added sugar intake such that BMI was more negatively correlated with hippocampal food-cue reactivity after glucose ingestion in individuals who consumed high levels of added sugar. Hippocampal BOLD was negatively correlated with prospective food intake.

The findings are consistent with the view that energy regulation involves hippocampal processes in humans and that added sugar and excess weight may impair this function.

The findings are consistent with the view that energy regulation involves hippocampal processes in humans and that added sugar and excess weight may impair this function.

The purpose of this study was to examine associations between self-reported weight history and sarcopenic obesity in adults with advanced knee osteoarthritis (OA).

Self-reported weight history was collected from n = 151 adults (58.9% female) with knee OA and BMI ≥30 kg/m

in a cross-sectional study. Body composition was assessed using dual-energy x-ray absorptiometry. Sarcopenic obesity was defined as appendicular skeletal muscle mass, adjusted by BMI, <0.51 kg/m

in females and <0.79 kg/m

in males; prevalence was 27.2%. Weight gain in the preceding year, weight gain ≥5% of body weight in the past decade, and multiple weight cycling events in life-span (loss of ≥10 lb [4.5 kg] with regain ≥3 times) were examined using logistic regression (adjusted by age, sex, and %fat mass), with the dependent variable of sarcopenic obesity presence.

Weight gain in the preceding year was associated with sarcopenic obesity (odds ratio [OR] 2.45, 95% CI 1.02-5.87). No associations were found with weight gain in the past decade (OR 1.04, 95% CI 0.43-2.5) or weight cycling (OR 0.86, 95% CI 0.37-2.01).

In adults with obesity and advanced knee OA, self-reported weight gain in the preceding year was associated with sarcopenic obesity. This patient population may benefit from recommendations that prioritize prevention of weight gain.

In adults with obesity and advanced knee OA, self-reported weight gain in the preceding year was associated with sarcopenic obesity. This patient population may benefit from recommendations that prioritize prevention of weight gain.

This study aimed to uncover genetic contributors to adiposity in early life.

A genome-wide association study of childhood body fatness in 34,401 individuals within the Nurses’ Health Studies and the Health Professionals Follow-up Study was conducted. Data were imputed to the 1000 Genomes Phase 3 version 5 reference panel.

A total of 1,354 single-nucleotide polymorphisms (P < 10

) were selected for replication in a previously published genome-wide association study of childhood BMI. Nineteen significant genome-wide (P < 5 × 10

) regions were observed, fourteen of which were previously associated with childhood obesity and five were novel BNDF (P = 7.58 × 10

), PRKD1 (P = 1.43 × 10

), 20p13 (P = 2.05 × 10

), FHIT (P = 1.77 × 10

), and LOC101927575 (P = 3.22 × 10

). The BNDF, FHIT, and PRKD1 regions were previously associated with adult BMI. LOC101927575 and 20p13 regions have not previously been associated with adiposity phenotypes. In a transcriptome-wide analysis, associations for POMC at 2p23.3 (P = 3.36 × 10

) and with TMEM18 at 2p25.3 (P = 3.53 × 10

) were observed. Childhood body fatness was genetically correlated with hip (r

= 0.42, P = 4.44 × 10

) and waist circumference (r

= 0.39, P = 5.56 × 10

), as well as age at menarche (r

= -0.37, P = 7.96 × 10

).

Additional loci that contribute to childhood adiposity were identified, further explicating its genetic architecture.

Additional loci that contribute to childhood adiposity were identified, further explicating its genetic architecture.Obesity is a chronic, multifactorial disease associated with a large number of comorbidities. check details The clinical management of obesity involves a stepwise integrated approach, beginning with behavioral and lifestyle modification, followed by antiobesity medications, endobariatric procedures, and bariatric surgery. Weight gain and subsequent obesity are common side effects of medications, such as prednisone or antipsychotics. In this era of precision medicine, it is essential to identify patients at the highest risk of weight gain as a result of medication use. Pharmacogenomics could play an important role in obesity management by optimizing use of antiobesity medications as well as minimizing adverse weight gain. This review aims to provide a comprehensive analysis of the current literature on the role of pharmacogenomics in obesity and medication-induced weight gain. In summary, there are more robust studies of medication associated with weight gain and pharmacogenomics, and more studies are needed to understand the role of pharmacogenomics in antiobesity medications.

Obesity is a major public health challenge, and the US military veteran population is disproportionately affected. Using deidentified records from a local weight management clinic and a national clinical data repository, obesity pharmacotherapy use and effectiveness for weight loss and obesity comorbidities in this vulnerable population were assessed.

During the initial year of the local clinic, 43 records with monthly follow-up of MOVE! lifestyle intervention augmented by obesity pharmacotherapy were found. Nationally, more than 2 million records of prescribed obesity pharmacotherapy compared with metformin as control were identified. Records with detailed documentation of weight trends from 1 year before to 1 year after the prescription date for further analysis were selected for review.

The most commonly prescribed medications in the local clinic were metformin, liraglutide, and combination phentermine/topiramate. On average, weight loss of -4.0 ± 2.1 kg over the initial 6-month intervention was observed.