Protein-restriction diet during the suckling phase programs rat metabolism against obesity and insulin resistance exacerbation induced by a high-fat diet in adulthood

Martins, Isabela Peixoto; Oliveira, Júlio Cézar de; Pavanello, Audrei; Matiusso, Camila Cristina Ianoni; Previate, Carina; Tófolo, Laize Peron; Ribeiro, Tatiane Aparecida; Franco, Claudinéia Conationi da Silva; Miranda, Rosiane Aparecida; Prates, Kelly Valério; Alves, Vander Silva; Francisco, Flávio Andrade; Moraes, Ana Maria Praxedes de; Malta, Ananda

doi:10.1016/j.jnutbio.2018.03.017

Cited by 17 publications

(13 citation statements)

References 51 publications

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“…This is the first demonstration of adult neurogenic hypertension programmed in the peri-pubertal period, while other studies have addressed the effect of low protein diet on blood pressure just after the exposure to the insult ( Loss et al, 2007 ; Penitente et al, 2007 ; Del Carmen Miñana-Solis and Escobar, 2008 ; Martins et al, 2011 ; Murca et al, 2012 ; Gomide et al, 2013 ; Penitente et al, 2014 ; Cappelli et al, 2018 ). In the context of DOHaD concept the studies have explored an earlier susceptible window of development, the peri-natal period ( Latorraca et al, 1998 ; De Oliveira et al, 2011 ; De Brito Alves et al, 2014 ; De Oliveira et al, 2014 ; Nascimento et al, 2014 ; Barros et al, 2015 ; De Oliveira et al, 2016 ; Ferreira et al, 2016 ; Paulino-Silva and Costa-Silva, 2016 ; Rossini et al, 2017 ; Barros et al, 2018 ; Martins et al, 2018 ; Assalin et al, 2019 ; Ferreira et al, 2019 ). The exact stimulus to the neurogenic hypertension is difficult to determine as the LP animals were hypophagic during the period of protein restriction, which also induced a caloric-restriction in peri-puberty, and a critical window of development ( De Oliveira et al, 2013 ; De Oliveira et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Protein Restriction in the Peri-Pubertal Period Induces Autonomic Dysfunction and Cardiac and Vascular Structural Changes in Adult Rats

et al. 2022

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Perturbations to nutrition during critical periods are associated with changes in embryonic, fetal or postnatal developmental patterns that may render the offspring more likely to develop cardiovascular disease in later life. The aim of this study was to evaluate whether autonomic nervous system imbalance underpins in the long-term hypertension induced by dietary protein restriction during peri-pubertal period. Male Wistar rats were assigned to groups fed with a low protein (4% protein, LP) or control diet (20.5% protein; NP) during peri-puberty, from post-natal day (PN) 30 until PN60, and then all were returned to a normal protein diet until evaluation of cardiovascular and autonomic function at PN120. LP rats showed long-term increased mean arterial pressure (p = 0.002) and sympathetic arousal; increased power of the low frequency (LF) band of the arterial pressure spectral (p = 0.080) compared with NP animals. The depressor response to the ganglion blocker hexamethonium was increased in LP compared with control animals (p = 0.006). Pulse interval variability showed an increase in the LF band and LF/HF ratio (p = 0.062 and p = 0.048) in LP animals. The cardiac response to atenolol and/or methylatropine and the baroreflex sensitivity were similar between groups. LP animals showed ventricular hypertrophy (p = 0.044) and increased interstitial fibrosis (p = 0.028) compared with controls. Reduced protein carbonyls (PC) (p = 0.030) and catalase activity (p = 0.001) were observed in hearts from LP animals compared with control. In the brainstem, the levels of PC (p = 0.002) and the activity of superoxide dismutase and catalase (p = 0.044 and p = 0.012) were reduced in LP animals, while the levels of GSH and total glutathione were higher (p = 0.039 and p = 0.038) compared with NP animals. Protein restriction during peri-pubertal period leads to hypertension later in life accompanied by sustained sympathetic arousal, which may be associated with a disorganization of brain and cardiac redox state and structural cardiac alteration.

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Section: Discussionmentioning

confidence: 99%

Protein Restriction in the Peri-Pubertal Period Induces Autonomic Dysfunction and Cardiac and Vascular Structural Changes in Adult Rats

et al. 2022

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“…Why this so opposite programming? [4][5][6][7] Although the increasing number of studies, the programming mechanisms and their impact on different windows remain unknown. Lactation is a very important postnatal window and any change in breast milk composition can seriously compromise the newborn health.…”

Section: Evidence Of Lactation As a Metabolic Programming Windowmentioning

confidence: 99%

“…For instance, protein restriction during infancy‐adolescence programs adult rat offspring to obesity and cardiometabolic dysfunctions, while during lactation it apparently programs to a lean phenotype. Why this so opposite programming? 4‐7 Although the increasing number of studies, the programming mechanisms and their impact on different windows remain unknown. Lactation is a very important postnatal window and any change in breast milk composition can seriously compromise the newborn health.…”

Section: Evidence Of Lactation As a Metabolic Programming Windowmentioning

confidence: 99%

Lactation as a programming window for metabolic syndrome

Picó

Reis

Egas

et al. 2021

Eur J Clin Investigation

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The concept of developmental origins of health and disease (DOHaD) was initially supported by the low birth weight and higher risk of developing cardiovascular disease in adult life, caused by nutrition restriction during foetal development. However, other programming windows have been recognized in the last years, namely lactation, infancy, adolescence and even preconception. Although the concept has been developed in order to study the impact of foetal calorie restriction in adult life, it is now recognized that maternal overweight during programming windows is also harmful to the offspring. This article explores and summarizes the current knowledge about the impact of maternal obesity and obesogenic diets during lactation in the metabolic programming towards the development of metabolic syndrome in the adult life. The impact of maternal obesity and obesogenic diets in milk quality is discussed, including the alterations in specific micro and macronutrients, as well as the impact of such alterations in the development of metabolic syndrome-associated features in the newborn, such as insulin resistance and adiposity. Moreover, the impact of milk quality and formula feeding in infants' gut microbiota, immune system maturation and in the nutrient-sensing mechanisms, namely those related to gut hormones and leptin, are also discussed under the current knowledge.

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“…Lactation is a window of susceptibility due to the development and maturation of major organs and tissues, which determine the offspring’s metabolic phenotype ( 2 , 15 ). Thus, exposure to undernutrition during this period can affect metabolism and pancreatic function.…”

Section: Introductionmentioning

confidence: 99%

“…Thus, exposure to undernutrition during this period can affect metabolism and pancreatic function. Our research group showed that a low-protein diet during lactation increased glycemia, even though offspring displayed higher peripheral insulin sensitivity and lower fasting insulinemia ( 15 ). Insulin is a major anabolic hormone involved in hepatic metabolism and dietary protein malnutrition can induce hepatic fat accumulation ( 16 ).…”

Section: Introductionmentioning

confidence: 99%

Protein restriction during lactation causes transgenerational metabolic dysfunction in adult rat offspring

Vargas

Martins²,

Matiusso³

et al. 2023

Front. Nutr.

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IntroductionProtein restriction during lactation can induce metabolic dysfunctions and has a huge impact on the offspring’s phenotype later in its life. We tested whether the effects of a maternal low-protein diet (LP) in rats can be transmitted to the F2 generation and increase their vulnerability to dietary insults in adulthood.MethodsFemale Wistar rats (F0) were fed either a low-protein diet (LP; 4% protein) during the first 2 weeks of lactation or a normal-protein diet (NP; 23% protein). The female offspring (F1 generation) were maintained on a standard diet throughout the experiment. Once adulthood was reached, female F1 offspring from both groups (i.e., NP-F1 and LP-F1) were bred to proven males, outside the experiment, to produce the F2 generation. Male F2 offspring from both groups (NP-F2 and LP-F2 groups) received a standard diet until 60 days old, at which point they received either a normal fat (NF; 4.5% fat) or a high fat diet (HF; 35% fat) for 30 days.ResultsAt 90 days old, LPNF-F2 offspring had increased lipogenesis and fasting insulinemia compared to NPNF-F2, without alteration in insulin sensitivity. HF diet caused increased gluconeogenesis and displayed glucose intolerance in LPHF-F2 offspring compared to LPNF-F2 offspring. Additionally, the HF diet led to damage to lipid metabolism (such as steatosis grade 3), higher body weight, fat pad stores, and hepatic lipid content.DiscussionWe concluded that an F0 maternal protein restricted diet during lactation can induce a transgenerational effect on glucose and liver metabolism in the F2 generation, making the offspring’s liver more vulnerable to nutritional injury later in life.

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Protein-restriction diet during the suckling phase programs rat metabolism against obesity and insulin resistance exacerbation induced by a high-fat diet in adulthood

Cited by 17 publications

References 51 publications

Protein Restriction in the Peri-Pubertal Period Induces Autonomic Dysfunction and Cardiac and Vascular Structural Changes in Adult Rats

Protein Restriction in the Peri-Pubertal Period Induces Autonomic Dysfunction and Cardiac and Vascular Structural Changes in Adult Rats

Lactation as a programming window for metabolic syndrome

Protein restriction during lactation causes transgenerational metabolic dysfunction in adult rat offspring

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