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Hunger and appetite are associated with fluctuations in glucose levels through mechanisms that remain incompletely understood. Hunger elicits epigastric sensations (“hunger pain”) that coincide with rhythmic gastric contractions, which intensify during hypoglycemia. These observations led to the glucostatic hypothesis, which proposed that glucose availability and utilization regulate food intake. Subsequent studies demonstrated that dynamic changes in blood glucose levels precede meal initiation and influence feeding behavior. Together, these findings provided early evidence for a physiological link between glycemia and appetite regulation.

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Pregnancy precipitates metabolic imbalance and accelerates death in an animal model of mitochondrial cardiomyopathy

Nicole M. Sayles, Gabriella Casalena, Dazhi Zhao, Ryan W. Dellinger, ... Giovanni Manfredi

Pregnancy precipitates metabolic imbalance and accelerates death in an animal model of mitochondrial cardiomyopathy

During pregnancy, the heart undergoes major physiological and metabolic changes to increase cardiac workload, and the demand for energy production is especially elevated during the trial of labor. Normally, cardiac structure and metabolism revert to the pre-pregnancy state shortly after delivery. However, in some cases, peripartum/postpartum cardiomyopathy (PPCM) occurs, which increases a person's risk of major cardiac events following pregnancy. The molecular mechanisms underlying PPCM remain poorly understood. In this study, we investigate the transcriptional, metabolic, and bioenergetic profiles of postpartum (PP) hearts in a mouse model of cardiomyopathy caused by the pathogenic p.S55L mutation in the mitochondrial protein coiled-coil-helix-coiled-coil-helix domain containing 10 (CHCHD10). Heterozygote p.S55L mutant CHCHD10 mice develop acute heart failure during the immediate PP period. We observe cardiac remodeling, mitochondrial stress, and profound metabolic rewiring in PP mutant CHCHD10 hearts. Metabolic rewiring results in decreased levels of heme and the depletion of key cofactors of energy metabolism, including NAD(H) and ADP. These findings suggest that mutant CHCHD10 hearts fail to meet the increased energy demands associated with the trial of labor due to the insufficient turnover rate of NAD+/NADH and ADP/ATP. We propose that this metabolic insufficiency drives PP mortality in mutant CHCHD10 mice. In support of this hypothesis, dietary supplementation with nicotinamide riboside and pterostilbene, a naturally derived polyphenol, increased PP survival and cardiac energy metabolites in mutant CHCHD10 mice. Our work provides novel insights into the molecular mechanisms of PP cardiomyopathy associated with mitochondrial stress and suggests potential benefits of dietary NAD(H) supplementation.

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Pregnancy precipitates metabolic imbalance and accelerates death in an animal model of mitochondrial cardiomyopathy

Nicole M. Sayles, Gabriella Casalena, Dazhi Zhao, Ryan W. Dellinger, ... Giovanni Manfredi

Pregnancy precipitates metabolic imbalance and accelerates death in an animal model of mitochondrial cardiomyopathy

During pregnancy, the heart undergoes major physiological and metabolic changes to increase cardiac workload, and the demand for energy production is especially elevated during the trial of labor. Normally, cardiac structure and metabolism revert to the pre-pregnancy state shortly after delivery. However, in some cases, peripartum/postpartum cardiomyopathy (PPCM) occurs, which increases a person's risk of major cardiac events following pregnancy. The molecular mechanisms underlying PPCM remain poorly understood. In this study, we investigate the transcriptional, metabolic, and bioenergetic profiles of postpartum (PP) hearts in a mouse model of cardiomyopathy caused by the pathogenic p.S55L mutation in the mitochondrial protein coiled-coil-helix-coiled-coil-helix domain containing 10 (CHCHD10). Heterozygote p.S55L mutant CHCHD10 mice develop acute heart failure during the immediate PP period. We observe cardiac remodeling, mitochondrial stress, and profound metabolic rewiring in PP mutant CHCHD10 hearts. Metabolic rewiring results in decreased levels of heme and the depletion of key cofactors of energy metabolism, including NAD(H) and ADP. These findings suggest that mutant CHCHD10 hearts fail to meet the increased energy demands associated with the trial of labor due to the insufficient turnover rate of NAD+/NADH and ADP/ATP. We propose that this metabolic insufficiency drives PP mortality in mutant CHCHD10 mice. In support of this hypothesis, dietary supplementation with nicotinamide riboside and pterostilbene, a naturally derived polyphenol, increased PP survival and cardiac energy metabolites in mutant CHCHD10 mice. Our work provides novel insights into the molecular mechanisms of PP cardiomyopathy associated with mitochondrial stress and suggests potential benefits of dietary NAD(H) supplementation.

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13th
Helmholtz Diabetes Conference 
Munich, 21-23. Sep 2026                                                                                                                             

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