Maternal High-Fat Diet Exposure During Gestation and Lactation Affects Intestinal Development in Suckling Rats.

Maternal health and diet influence metabolic status and play a crucial role in the development of metabolic function in offspring and their susceptibility to metabolic diseases in adulthood. The pathogenesis of various metabolic disorders is often associated with impairment in intestinal structure and function. Thus, the aim of the current study was to determine the effects of maternal exposure to a high fat diet (HFD), during gestation and lactation, on small intestinal growth and maturation in rat pups at 21 days old. Female, Wistar Han rats were fed either a breeding diet (BD) or high fat diet (HFD), from mating until the 21st day of lactation. Maternal HFD exposure increased body weight, BMI and adiposity. Compared to the maternal BD, HFD exposure influenced small intestine histomorphometry in a segment-dependent manner, changed the activity of brush border enzymes and had an impact on intestinal contractility via changes in cholinergic signaling. Moreover, offspring from the maternal HFD group had upregulated mRNA expression of cyclooxygenase (COX)-2, which plays a role in the inflammatory process. These results suggest that maternal HFD exposure, during gestation and lactation, programs the intestinal development of the offspring in a direction toward obesity as observed changes are also commonly reported in models of diet-induced obesity. The results also highlight the importance of maternal diet preferences in the process of developmental programming of metabolic diseases.

Small intestinal development in suckling rats after enteral obestatin administration.

This study investigated the effect of enteral administration of obestatin on the development of small intestine, as well as oxidative stress markers and trancriptomic profile of gastrointestinal genes. Suckling rats were assigned to 3 groups treated with: C-saline solution; OL-obestatin (125 nmol/kg BW); OH-obestatin (250 nmol/kg BW) administered twice daily, from the 14th to the 21st day of life. Enteral administration of obestatin in both studied doses had no effect neither on the body weight of animals nor the BMI calculated in the day of euthanasia. Compared to the control group (C), treatment with obestatin resulted in significant changes in the histometry of the small intestinal wall as well as intestinal epithelial cell remodeling. The observed changes and their possible implications for intestinal development were dependent on the dosage of peptide. The enteral administration of high dose (OH) of obestatin significantly decreased its expression in the stomach and increased markers of oxidative stress. The gene profile revealed MAPK3 (mitogen-activated protein kinase-3) as the key regulator gene for obestatin action in the gastrointestinal track. In conclusion, we have showed that enteral administration of obestatin influences the gut mucosa remodeling. It is also suggested that the administration of high dose (OH) has inhibitory effect on the intestinal maturation of suckling rats.

Small intestine motility development in newborn mammals.

Since the beginning of the 20th century, researchers have been working to improve the understanding of gastrointestinal motility. The first major discovery was the observation of a migrating myoelectric complex that turned out to be a universal occurrence among vertebrates. Further inquires resulted in a detailed description of its development during different stages of ontogeny. Some time before that, a cornerstone had been laid for a breakthrough that would come years later. That cornerstone came in the form of interstitial cells of Cajal whose true role could not be discerned until the discovery of a CD117 receptor - their main marker. With the ability to precisely mark interstitial cells of Cajal, a wave of subsequent new experiments and observations connected them to the occurrence of slow waves and allowed an understanding of the mechanism responsible for their generation. Some of these findings suggested that Cajal cells might have a role in the development of several motility disorders thus opening an avenue of research that requires the usage of both traditional and advanced diagnostic methods.

The biological role of a-ketoglutaric acid in physiological processes and its therapeutic potential.

In this article we present the results of recent studies on the mechanism of action and biological role of α-ketoglutaric acid (AKG) in animals including developmental period of life. AKG is an intermediate in the Krebs cycle, which generates energy for life processes. Administration of AKG has been shown to be beneficial for proper development and function of the skeletal system during growth of young organisms, as well as in adulthood. In the form of a dietary supplement it also contributes to inhibition of osteoporosis in women. Moreover, it promotes the growth of muscle mass and accelerates wound healing. AKG has a significant impact on the morphology of the gastrointestinal tract in healthy animals and animals with damaged gastrointestinal tract mucosa. It is also a promising substance for the treatment of patients with short bowel syndrome, as it stimulates beneficial changes in intestinal morphology. Recent research has also revealed that AKG has neuroprotective effects.