Dietary analysis predicts that marginal Zn deficiency is common in women of reproductive age. The lack of reliable biomarkers limits the capacity to assess Zn status and consequently understand effects of maternal Zn deficiency. We determined effects of marginal maternal Zn deficiency on mammary gland function, milk secretion, and milk composition in mice. Mice (n = 12/diet) were fed marginal (ZD; 15 mg Zn/kg diet) or adequate (ZA; 30 mg Zn/kg diet) Zn diets for 30 d prior to conception through mid-lactation. Mice fed the ZD had a higher plasma Zn concentration (~20%; P < 0.05) but lower milk Zn concentration (~15%; P < 0.05) compared with mice fed the ZA. ZnT2 abundance was higher (P < 0.05) in mice fed the ZD compared with mice fed the ZA; no effect on ZnT4 abundance was detected. The Zn concentration of mammary gland mitochondria tended to be ~40% greater in mice fed ZD (P = 0.07); this was associated with apoptosis and lower milk secretion (~80%; P < 0.01). Total milk protein was ~25% higher (P < 0.05), although the abundance of the major milk proteins (caseins and whey acidic protein) was lower (P < 0.05) in mice fed the ZD. Proteomic analysis of milk proteins revealed an increase (P < 0.05) in four proteins in mice fed the ZD. These findings illustrate that marginal maternal Zn deficiency compromises mammary gland function and milk secretion and alters milk composition. This suggests that lactating women who consume inadequate Zn may not produce and/or secrete an adequate amount of high quality milk to provide optimal nutrition to their developing infant.
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http://dx.doi.org/10.3945/jn.111.150623 | DOI Listing |
Mol Metab
January 2025
Department of Internal Medicine, University of Michigan, Ann Arbor, MI USA; Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA. Electronic address:
Several groups of neurons in the NTS suppress food intake, including Prlh-expressing neurons (NTS cells). Not only does the artificial activation of NTS cells decrease feeding, but also the expression of Prlh (which encodes the neuropeptide PrRP) and neurotransmission by NTS neurons contributes to the restraint of food intake and body weight, especially in animals fed a high fat diet (HFD). We used animals lacking PrRP receptors GPR10 and/or GRP74 (encoded by Prlhr and Npffr2, respectively) to determine roles for each in the restraint of food intake and body weight by the increased expression of Prlh in NTS neurons (NTS mice) and in response to the anorectic PrRP analog, p52.
View Article and Find Full Text PDFJ Nutr
January 2025
Department of Physiology and Oral Physiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8553, Japan.
Background: Modern dietary trends have led to an increase in foods that are relatively high in n-6 polyunsaturated fatty acids (PUFAs) and low in n-3 PUFAs. We previously reported that the offspring of mother mice that consumed a diet high in n-6 linoleic acid (LA) and low in n-3 α-linolenic acid (ALA), hereinafter called the LA/ALA diet, exhibit behavioral abnormalities related to anxiety and feeding.
Objective: We currently lack a comprehensive overview of the behavioral abnormalities in these offspring, which was investigated in this study.
J Agric Food Chem
January 2025
Institute of Food Sciences and Technology, National Taiwan University, 10617 Taipei, Taiwan.
Obesity-induced muscle alterations, such as inflammation, metabolic dysregulation, and myosteatosis, lead to a decline in muscle mass and function, often resulting in sarcopenic obesity. Currently, there are no definitive treatments for sarcopenic obesity beyond lifestyle changes and dietary supplementation. Feruloylacetone (FER), a thermal degradation product of curcumin, and its analog demethoxyferuloylacetone (DFER), derived from the thermal degradation of bisdemethoxycurcumin, have shown potential antiobesity effects in previous studies.
View Article and Find Full Text PDFDiabetol Metab Syndr
January 2025
Laboratory of Immunopharmacology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation-Fiocruz, Campus Maré. Centro de Pesquisa, Inovação e Vigilância em Covid-19 e Emergências Sanitárias. Endereço: Av. Brasil, 4036-Bloco 2. Manguinhos, Rio de Janeiro, RJ, CEP 21040-361, Brazil.
Introduction: Metabolic syndrome (MetS) is a metabolic disorder related to obesity and insulin resistance and is the primary determinant of the development of low-intensity chronic inflammation. This continuous inflammatory response culminates in neuroimmune-endocrine dysregulation responsible for the metabolic abnormalities and morbidities observed in individuals with MetS. Events such as the accumulation of visceral adipose tissue, increased plasma concentrations of free fatty acids, tissue hypoxia, and sympathetic hyperactivity in individuals with MetS may contribute to the activation of the innate immune response, which compromises cerebral microcirculation and the neurovascular unit, leading to the onset or progression of neurodegenerative diseases.
View Article and Find Full Text PDFJ Transl Med
January 2025
Research Unit NeuroBiology of Diabetes, Helmholtz Munich, Ingolstädter Landstraße 1, 85764, Neuherberg, Germany.
Background: Obese subjects undergoing weight loss often fear the Yoyo dieting effect, which involves regaining or even surpassing their initial weight. To date, our understanding of such long-term obesity and weight cycling effects is still limited and often based on only short-term murine weight gain and loss studies. This study aimed to investigate the long-term impacts of weight cycling on glycemic control and metabolic health, focusing on adipose tissue, liver, and hypothalamus.
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