Metabolic syndrome (MetS) is a cluster of metabolic abnormalities that include insulin resistance, impaired glucose tolerance, dyslipidemia, hypertension, and abdominal obesity. Coffee production generates large quantities of waste products, which pose a serious threat to the environment. However, coffee by-products, such as coffee pulp (CP), possess an undeniable wealth of bioactive components. Based on this, we investigated whether a 10-week dietary intervention with 250 mg/kg/d of CP could prevent or ameliorate MetS in high-fructose-fed rats. Consumption of CP by rats fed a high-fructose diet reduced body weight gain, lowered systolic blood pressure (SBP), fasting plasma glucose and insulin levels, and improved insulin resistance compared to rats fed a high-fructose diet alone. At the hepatic level, CP attenuated the increase in lipid storage, reduced lipid peroxidation, and improved glutathione levels when combined with a high-fructose diet. CP also affected the expression of key genes related to glucose and lipid metabolism in hepatic and adipose tissues, in rats fed a fructose-rich diet. This study demonstrates that CP ameliorates several consequences of high-fructose-induced MetS in the rat (weight gain, hypertension, glucose intolerance, insulin resistance, changes in liver, and adipose tissue function). Hence, our data provide evidence that CP consumption in the context of a high-fructose diet can be used to improve MetS management.

Background: Obesity during pregnancy is associated with an elevated risk of severe COVID-19, including higher rates of maternal complications, intensive care admission, and adverse neonatal outcomes. The impact of combination of SARS-CoV-2 infection and maternal obesity in placental pathology has not been properly investigated. Aim: To compare the histopathological changes in the placenta induced by active SARS-CoV-2 infection in obese and non-obese patients. Methods: This retrospective cohort study included human placentas from non-obese women and pre-gestationally obese women with active SARS-CoV-2 infection (SARS and OB+SARS, respectively), and placentas from non-obese women and pre-gestationally obese women without SARS-CoV-2 infection (control and OB, collected in the post- and pre-pandemic periods, respectively). Results: A higher (50%) occurrence of ischemic injury and subchorionic fibrin deposits and a 15× higher risk of occurrence of these lesions were found in the OB+SARS group, in relation to control. In contrast, a 10% lower risk of developing chorangiosis in the OB+SARS group than the OB group was observed. Conclusions: An increased risk of lesions related to both maternal and fetal malperfusion and ischemic injury and a lower risk for chorangiosis exist in placentas from obese women affected by SARS-CoV-2 infection. Importantly, these differences were not observed in placentas from non-obese women.

Coffee pulp (CP) and silverskin (SSK), which ameliorate metabolic syndrome features induced by high-fructose feeding in rats, can modulate specific proteomic alterations in the hippocampus and hypothalamus induced by fructose.

By directly regulating nutrient supply and fetal growth, the placenta plays a central role in fetal programming. The extent to which SARS-CoV-2 maternal infection during pregnancy will affect the long-term metabolic health of the newborn is yet to be explored. As trophoblast cells express the ACE2 (angiotensin converting enzyme 2) receptor, we aimed to investigate the potential fetal programming effects of SARS-CoV-2 Spike protein S1 subunit (Spike S1), by focusing on nutrient transport. We investigated the in vitro effect of Spike S1 (100 ng/mL; 24 h) on two in vitro models of human trophoblasts, primary cultured human trophoblasts and the BeWo cell line. Spike S1 elicited an inflammatory response, caused a low grade cytotoxic and antiproliferative effect and, in the more actively replicating BeWo cell line, induced G2-M cell cycle arrest. Moreover, it interfered with the activities of the glucose transporter GLUT1 (facilitative glucose transporter 1) and the folic acid transporter RFC1 (reduced folate carrier 1), and altered the gene expression of the amino acid transporters LAT1 (L-type amino acid transporter 1) and y⁺LAT2 (y⁺L-type amino acid transporter 2). It also markedly increased mTOR (mammalian target of rapamycin) gene expression in primary cultured trophoblasts. We conclude that the Spike S1 subunit induces some changes in trophoblast metabolic parameters that may be of relevance for fetal programming metabolic disease in the adult.