scholarly journals An endocrine hypothesis to explain obesity-related lactation insufficiency in breastfeeding mothers

2020 ◽  
Vol 87 (1) ◽  
pp. 78-81
Author(s):  
Christopher H. Knight

AbstractIn this Research Reflection I shall develop and validate the hypothesis that lactation insufficiency in obese breastfeeding mothers has an endocrine explanation. I shall not present data, but I shall review pertinent literature to show that obesity is associated with a partial or sometimes complete failure to initiate and maintain lactation, and critically examine the belief that this is due to psychosocial factors, a failure of prolactin secretion or both. Since progesterone is inhibitory to lactogenesis and oestrogens are inhibitory to milk secretion, I shall then explore the possibility that these steroids are linked to lactation failure, through sequestration of progesterone and aromatization of oestrogen in mammary adipose tissue. I shall conclude by describing experimental approaches in animal models that could be used to test this hypothesis.

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1412
Author(s):  
Katarzyna Piotrowska ◽  
Maciej Tarnowski

In recent years, adipose tissue has attracted a lot of attention. It is not only an energy reservoir but also plays important immune, paracrine and endocrine roles. BMAT (bone marrow adipose tissue) is a heterogeneous tissue, found mostly in the medullary canal of the long bones (tibia, femur and humerus), in the vertebrae and iliac crest. Adipogenesis in bone marrow cavities is a consequence of ageing or may accompany pathologies like diabetes mellitus type 1 (T1DM), T2DM, anorexia nervosa, oestrogen and growth hormone deficiencies or impaired haematopoiesis and osteoporosis. This paper focuses on studies concerning BMAT and its physiology in dietary interventions, like obesity in humans and high fat diet in rodent studies; and opposite: anorexia nervosa and calorie restriction in animal models.


2010 ◽  
pp. 633-644 ◽  
Author(s):  
Y Wang ◽  
U Wisloff ◽  
OJ Kemi

Exercise training-induced cardiac hypertrophy occurs following a program of aerobic endurance exercise training and it is considered as a physiologically beneficial adaptation. To investigate the underlying biology of physiological hypertrophy, we rely on robust experimental models of exercise training in laboratory animals that mimic the training response in humans. A number of experimental strategies have been established, such as treadmill and voluntary wheel running and swim training models that all associate with cardiac growth. These approaches have been applied to numerous animal models with various backgrounds. However, important differences exist between these experimental approaches, which may affect the interpretation of the results. Here, we review the various approaches that have been used to experimentally study exercise training-induced cardiac hypertrophy; including the advantages and disadvantages of the various models.


2016 ◽  
Vol 144 (3) ◽  
pp. 409 ◽  
Author(s):  
Vajreswari Ayyalasomayajula ◽  
SivaSankara Vara Prasad Sakamuri ◽  
UdayKumar Putcha ◽  
GiridharanNappan Veettil

2019 ◽  
Vol 242 (1) ◽  
pp. T81-T94 ◽  
Author(s):  
Clare M Reynolds ◽  
Mark H Vickers

Alterations in the environment during critical periods of development, including altered maternal nutrition, can increase the risk for the development of a range of metabolic, cardiovascular and reproductive disorders in offspring in adult life. Following the original epidemiological observations of David Barker that linked perturbed fetal growth to adult disease, a wide range of experimental animal models have provided empirical support for the developmental programming hypothesis. Although the mechanisms remain poorly defined, adipose tissue has been highlighted as playing a key role in the development of many disorders that manifest in later life. In particular, adipokines, including leptin and adiponectin, primarily secreted by adipose tissue, have now been shown to be important mediators of processes underpinning several phenotypic features associated with developmental programming including obesity, insulin sensitivity and reproductive disorders. Moreover, manipulation of adipokines in early life has provided for potential strategies to ameliorate or reverse the adverse sequalae that are associated with aberrant programming and provided insight into some of the mechanisms involved in the development of chronic disease across the lifecourse.


1962 ◽  
Vol 202 (3) ◽  
pp. 465-468 ◽  
Author(s):  
Carlos Beyer ◽  
Flavio Mena ◽  
Pablo Pacheco ◽  
Manuel Alcaraz

The effect of brain-stem lesions on lactation in the cat was studied. Lesions in the rostral mesencephalon or caudal hypothalamus, which involved the dorsal longitudinal fasciculus, caused persistent supression of milk secretion and involution of the mammary glands. This effect seems to be due to interruption of the afferent pathway for prolactin secretion. Control lesions in other parts of the brain caused only a transient impairment of lactation.


1993 ◽  
Vol 44 (3) ◽  
pp. 509 ◽  
Author(s):  
TB Mepham

The author has reviewed the development of theories, over the last century, on the role of glucose in mammary metabolism, focusing on three overlapping issues, via. the extent of glucose utilization by mammary tissue, the synthesis of lactose, and the way in which glucose supply controls secretion of the aqueous phase of milk. In the first half of the century, deficiencies in technique produced several misleading results, and later progress resulted largely from methodological advances. Methodology has also been important in shaping research programmes, as is evident in the current emphasis on techniques of molecular biology. However, the review indicates the importance of employing a combination of experimental approaches, including whole-animal studies. Through the adoption of such approaches, it is now appreciated that glucose plays a key role in regulating lactation. It is suggested that developments over the last 30 years, which have led to formulation of an apparently resilient theory of milk secretion, conform to the notion of a 'progressive research programme' built on a 'positive heuristic', as proposed by the philosopher of science, I. Lakatos.


Author(s):  
Marilia C.L. Seelaender ◽  
Miguel Luiz Batista

AbstractAdipose tissue inflammation plays a role in the etiology of many chronic diseases, and has been the focus of much attention in the context of obesity and metabolic syndrome. Similarly, during cancer cachexia, a syndrome that markedly increases cancer-associated morbidity and mortality, local adipose inflammation is reported in animal models and in patients, potentially contributing to the chronic systemic inflammation that constitutes the hallmark of this condition. We discuss, on the basis of information generated by obesity-related studies, the possible relation between adipose tissue inflammation and compromised steroid hormone secretion and action in cachexia.


2008 ◽  
Vol 2008 ◽  
pp. 1-14 ◽  
Author(s):  
David M. Miller ◽  
Thomas B. Thornley ◽  
Dale L. Greiner ◽  
Aldo A. Rossini

Transplantation of allogeneic organs has proven to be an effective therapeutic for a large variety of disease states, but the chronic immunosuppression that is required for organ allograft survival increases the risk for infection and neoplasia and has direct organ toxicity. The establishment of transplantation tolerance, which obviates the need for chronic immunosuppression, is the ultimate goal in the field of transplantation. Many experimental approaches have been developed in animal models that permit long-term allograft survival in the absence of chronic immunosuppression. These approaches function by inducing peripheral or central tolerance to the allograft. Emerging as some of the most promising approaches for the induction of tolerance are protocols based on costimulation blockade. However, as these protocols move into the clinic, there is recognition that little is known as to their safety and efficacy when confronted with environmental perturbants such as virus infection. In animal models, it has been reported that virus infection can prevent the induction of tolerance by costimulation blockade and, in at least one experimental protocol, can lead to significant morbidity and mortality. In this review, we discuss how viruses modulate the induction and maintenance of transplantation tolerance.


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