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Purpose: Obesity may alter the severity of infection with Coronavirus disease 2019 (COVID-19). Age may impact the association between body weight and severity of COVID-19 in patients with obesity. The aim of the study was to examine the association between obesity and severity of infection in a Danish cohort hospitalized with COVID-19 in the initial wave of the pandemic. Patients and methods: Based on data from the nationwide, clinical database: COVID-DK, risks of intensive care unit (ICU) admission, invasive mechanical ventilation (IMV), and mortality were compared among patients with and without obesity. Interaction with age was examined and we used Inverse Probability of Treatment Weighting regression for confounder adjustment. Results: Among 524 patients, 142 (27%) were admitted to the ICU, 112 (21%) required IMV, and 109 (21%) died. Compared to COVID-19 patients without obesity, patients with obesity displayed a non-significant increased risk of ICU admission (Relative Risk [RR] 1.19, 95% Confidence Interval [CI] 0.88; 1.60), IMV (RR 1.23, CI 0.86; 1.75) and mortality (RR 1.21, CI 0.84; 1.75). COVID-19 patients with obesity, <60 years had highly increased risk of ICU admission (RR 1.92, CI 1.14; 3.24) and IMV (RR 1.95, CI 1.09; 3.49). Conclusions: In hospitalized COVID-19 patients, obesity conferred an approximately 20% increased risk for ICU admission, IMV, and death, although these relationships did not reach statistical significance. COVID-19 patients with obesity and <60 years had an almost doubled risk of ICU admission and IMV.

A healthy diet is essential to prevent childhood obesity, however, adherence to a healthy diet is challenging. The aim of this study was to give a comprehensive overview of the literature investigaating associations between food and beverages and overweight/obesity in children and adolescents in order to identify dietary risk factors. A systematic search was performed in four databases and observational studies were included. Meta-analysis was performed using the random effect model. Sixty records met inclusion criteria and 14 different food or beverage categories were identified. A higher intake of sugar-sweetened beverages increased the odds of overweight/obesity by 1.20 (p < 0.05) (n = 26) and higher intake of fast food increased the odds of overweight/obesity by 1.17 (p < 0.05) (n = 24). Furthermore, higher intake of meat (OR 1.02, p < 0.05 (n:7)) and refined grains (OR 1.28, p < 0.05 (n:3)) was associated with an increased risk of overweight/obesity. In contrast, higher intake of whole grain (OR 0.86, p = 0.04 (n:5)) and more surprisingly sweet bakery (OR 0.59, p < 0.05 (n:3)) was associated with a decreased risk of overweight/obesity. In conclusion, a higher intake of sugar-sweetened beverages and a higher intake of fast food was identified as the primary dietary risk factors for overweight/obesity. Future research is needed to strengthen the generalizability of these results.

BACKGROUND: High carbohydrate, i.e., sugars, intake potentially drives the liver into a lipogenic state leading to elevated plasma fatty acids. Excessive intake of saturated fat and sugar-sweetened soda induces liver fat accumulation, but studying the effect of high intake from sugar-sweetened soda on the de novo lipogenesis (DNL) fatty acids in long-term randomized trials is lacking. OBJECTIVE: To study the effect of consuming 1 L/day of sugar-sweetened soda, semi-skimmed milk (milk), aspartame-sweetened soda or water over 24 weeks on DNL-derived fatty acids (i.e., palmitate (primary outcome) and other saturated and monounsaturated fatty acids), and markers of stearoyl-CoA desaturase activity (SCD1) in plasma phospholipids (PL), cholesteryl esters (CE), and triglycerides (TG). DESIGN AND METHODS: A randomized parallel study was conducted simultaneously at Aarhus University Hospital and Copenhagen University, Denmark, including (n = 41) individuals aged 20-50 years, with BMI of 26-40 kg/m2, and without diabetes. The groups consisted of 9 individuals in the sugar-sweetened soda, 10 in the milk, 11 in the aspartame-sweetened soda, and 11 in the water. The change at 24 weeks was assessed and compared across the groups using ANCOVA and mixed-effects models. Correlations of fatty acid changes with liver fat accumulation (magnetic resonance imaging) were explored. RESULTS: After 24 weeks, the groups differed in palmitate proportions in PL, oleate in CE and PL, and palmitoleate and SCD1 in all fractions (p < 0.05). Compared with water, the relative proportion of palmitate in PL increased by approximately 1% during both sugar-sweetened soda (p = 0.011) and milk (p = 0.006), whereas oleate and palmitoleate increased only during sugar-sweetened soda (CE 2.77%, p < 0.001; PL 1.51%, p = 0.002 and CE 1.46%, PL 0.24%, TG 1.31%, all p < 0.001, respectively). Liver fat accumulation correlated consistently with changes in palmitoleate, whereas correlations with palmitate an

Background: High carbohydrate, i.e., sugars, intake potentially drives the liver into a lipogenic state leading to elevated plasma fatty acids. Excessive intake of saturated fat and sugar-sweetened soda induces liver fat accumulation, but studying the effect of high intake from sugar-sweetened soda on the de novo lipogenesis (DNL) fatty acids in long-term randomized trials is lacking. Objective: To study the effect of consuming 1 L/day of sugar-sweetened soda, semi-skimmed milk (milk), aspartame-sweetened soda or water over 24 weeks on DNL-derived fatty acids (i.e., palmitate (primary outcome) and other saturated and monounsaturated fatty acids), and markers of stearoyl-CoA desaturase activity (SCD1) in plasma phospholipids (PL), cholesteryl esters (CE), and triglycerides (TG). Design and methods: A randomized parallel study was conducted simultaneously at Aarhus University Hospital and Copenhagen University, Denmark, including (n = 41) individuals aged 20-50 years, with BMI of 26-40 kg/m(2), and without diabetes. The groups consisted of 9 individuals in the sugar-sweetened soda, 10 in the milk, 11 in the aspartame-sweetened soda, and 11 in the water. The change at 24 weeks was assessed and compared across the groups using ANCOVA and mixed-effects models. Correlations of fatty acid changes with liver fat accumulation (magnetic resonance imaging) were explored. Results: After 24 weeks, the groups differed in palmitate proportions in PL, oleate in CE and PL, and palmitoleate and SCD1 in all fractions (p < 0.05). Compared with water, the relative proportion of palmitate in PL increased by approximately 1% during both sugar-sweetened soda (p = 0.011) and milk (p = 0.006), whereas oleate and palmitoleate increased only during sugar-sweetened soda (CE 2.77%, p < 0.001; PL 1.51%, p = 0.002 and CE 1.46%, PL 0.24%, TG 1.31%, all p < 0.001, respectively). Liver fat accumulation correlated consistently with changes in palmitoleate, whereas correlations with palmitate

PURPOSE: Brown adipose tissue (BAT) activation in humans has gained interest as a potential target for treatment of obesity and insulin resistance. In rodents, BAT is primarily induced through beta-3 adrenergic receptor (ADRB3) stimulation, whereas the primary beta adrenergic receptors (ADRBs) involved in human BAT activation are debated. We evaluated the importance of different ADRB subtypes for uncoupling protein 1 (UCP1) induction in human brown adipocytes. METHODS: A human BAT cell model (TERT-hBA) was investigated for subtype-specific ADRB agonists and receptor knockdown on UCP1 mRNA levels and lipolysis (glycerol release). In addition, fresh human BAT biopsies and TERT-hBA were evaluated for expression of ADRB1, ADRB2, and ADRB3 using RT-qPCR. RESULTS: The predominant ADRB subtype in TERT-hBA adipocytes and BAT biopsies was ADRB1. In TERT-hBA, UCP1 mRNA expression was stimulated 11.0-fold by dibutyryl cAMP (dbcAMP), 8.0-fold to 8.4-fold by isoproterenol (ISO; a pan-ADRB agonist), and 6.1-fold to 12.7-fold by dobutamine (ADRB1 agonist), whereas neither procaterol (ADRB2 agonist), CL314.432, or Mirabegron (ADRB3 agonists) affected UCP1. Similarly, dbcAMP, ISO, and dobutamine stimulated glycerol release, whereas lipolysis was unaffected by ADRB2 and ADRB3 agonists. Selective knockdown of ADRB1 significantly attenuated ISO-induced UCP1 expression. CONCLUSION: The adrenergic stimulation of UCP1 and lipolysis may mainly be mediated through ADRB1. Moreover, ADRB1 is the predominant ADRB in both TERT-hBA and human BAT biopsies. Thus, UCP1 expression in human BAT may, unlike in rodents, primarily be regulated by ADRB1. These findings may have implications for ADRB agonists as future therapeutic compounds for human BAT activation.

Svær overvægt bør være et bredt fælles ansvar, der ikke kun er overladt til individet selv. Derfor er det også tid til en politisk erkendelse af behovet for en national handlingsplan for svær overvægt, skriver 10 læger og eksperter, som er medlemmer af Overvægtsalliancen.

Since publication the authors noticed an error in Tables 2, 3, and 4 of the original article, where the pre-intervention values were presented by mean and SD instead of mean and SE as described in the table text. The correct tables are reproduced below where SD's are replaced by SE's.

Aims: To examine the nationwide trends in antidiabetic drug utilization and expenditure in Denmark over the past 22 years. Methods: Data on antidiabetic use and expenditure from 1996 to 2017 were retrieved from the Register of Medicinal Product Statistics. Antidiabetic drug use is reported as defined daily dose (DDD) in total counts and per 1000 inhabitants/d. Expenditure is reported as volume sold in total counts per 1000 inhabitants and as annual mean expenditure. Results: Throughout the study period, the total use of antidiabetic drugs increased from 16.4 to 55.8 DDDs per 1000 inhabitants/d, while total expenditure increased from €59 to €286 m. The introduction of glucagon-like peptide-1 receptor agonists (GLP-1RAs), dipeptidyl peptidase-4 inhibitors and sodium-glucose co-transporter-2 inhibitors has, since 2005, led to considerable variation in the proportional use of the different drug classes. Use of insulin and insulin analogues accounted for the majority of the cost of antidiabetic drugs, peaking at 75% in 2008; however, its proportional impact on overall antidiabetic drug expenditure decreased to ~44% in 2017. In contrast, a steep increase in GLP-1RA expenditure was observed from 2010 to 2017, reaching an annual cost of €85 m (~29% of all antidiabetic expenditure). Conclusion: Antidiabetic drug utilization and cost in Denmark has increased considerably over the last 22 years, in accordance with the increased incidence of type 2 diabetes and changes in treatment guidelines. The release of several novel antidiabetic drugs seems to be responsible for the increase in antidiabetic drug expenditure.