Cover Story Current Issue
Despite intensive drug development efforts and public health initiatives, obesity is increasing in incidence and predicted to affect over 50% of all adults worldwide by 2035. Being chronically overweight increases the risk of serious disease co-morbidities that, in turn, increase mortality and healthcare costs. Behavioral approaches to combat obesity, such as diet and exercise, rarely produce lasting weight loss commonly due to compensatory hyperphagia and hypometabolism. These limitations have stimulated interest in pharmacotherapies that target gut-derived peptide hormones involved in the regulation of energy homeostasis, such as PYY, GIP, CCK, and GLP-1. These peptides are secreted by different enteroendocrine cells distributed throughout the intestine in response to food intake, subsequently enhancing satiation signaling and ultimately promotes meal termination. However, a major challenge of FDA-approved and experimental weight-loss medications that target GI-derived satiation signals is the frequent occurrence of nausea and vomiting.
Current Issue
Loss of energy homeostasis contributes to hepatic damage development in sickle cell disease
Loss of energy homeostasis contributes to hepatic damage development in sickle cell disease
Sickle cell disease (SCD) is characterized by the expression of an abnormal hemoglobin variant (HbS) that promotes distortion and early destruction of red blood cells, resulting in hemolytic anemia, vaso-occlusive crisis, ischemia and, ultimately, tissue damage. Hepatic function is specially compromised in SCD patients; however, the underlying pathological mechanisms remain largely unknown. In the current study, we confirmed the presence of hepatic damage in a murine model of SCD and, through a label free quantitative proteomic approach, we identified significant alterations in protein expression compared to healthy controls. These changes unveiled distinct proteome expression profiles between groups, with molecular alterations linked to impaired hepatic function, anemia, mitochondrial dysfunction, and alteration in lipid metabolism. We also confirmed these novel alterations through molecular and functional analyses, revealing a previously undescribed liver energy homeostasis imbalance, accompanied by accumulation of foam cells. Our findings provide new insights into the complex mechanisms underlying liver disease and potential therapeutic targets in SCD.
Articles in Press
Loss of energy homeostasis contributes to hepatic damage development in sickle cell disease
Loss of energy homeostasis contributes to hepatic damage development in sickle cell disease
Sickle cell disease (SCD) is characterized by the expression of an abnormal hemoglobin variant (HbS) that promotes distortion and early destruction of red blood cells, resulting in hemolytic anemia, vaso-occlusive crisis, ischemia and, ultimately, tissue damage. Hepatic function is specially compromised in SCD patients; however, the underlying pathological mechanisms remain largely unknown. In the current study, we confirmed the presence of hepatic damage in a murine model of SCD and, through a label free quantitative proteomic approach, we identified significant alterations in protein expression compared to healthy controls. These changes unveiled distinct proteome expression profiles between groups, with molecular alterations linked to impaired hepatic function, anemia, mitochondrial dysfunction, and alteration in lipid metabolism. We also confirmed these novel alterations through molecular and functional analyses, revealing a previously undescribed liver energy homeostasis imbalance, accompanied by accumulation of foam cells. Our findings provide new insights into the complex mechanisms underlying liver disease and potential therapeutic targets in SCD.
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