Effect of developmental NMDAR antagonism with CGP 39551 on aspartame-induced hypothalamic and adrenal gene expression.

Rationale: Aspartame (L-aspartyl phenylalanine methyl ester) is a non-nutritive sweetener (NNS) approved for use in more than 6000 dietary products and pharmaceuticals consumed by the general public including adults and children, pregnant and nursing mothers. However a recent prospective study reported a doubling of the risk of being overweight amongst 1-year old children whose mothers consumed NNS-sweetened beverages daily during pregnancy. We have previously shown that chronic aspartame (ASP) exposure commencing in utero may detrimentally affect adulthood adiposity status, glucose metabolism and aspects of behavior and spatial cognition, and that this can be modulated by developmental N-methyl-D-aspartate receptor (NMDAR) blockade with the competitive antagonist CGP 39551 (CGP).

Differential effects of early-life NMDA receptor antagonism on aspartame-impaired insulin tolerance and behavior.

Unlabelled: We have previously showed that lifetime exposure to aspartame, commencing in utero via the mother's diet, may impair insulin tolerance and cause behavioral deficits in adulthood via mechanisms which are incompletely understood. The role of the CNS in regulating glucose homeostasis has been highlighted by recent delineation of the gut-brain axis, in which N-methyl-d-aspartic acid receptors (NMDARs) are important in maintaining glucose homeostasis, in addition to regulating certain aspects of behavior. Since the gut-brain axis can be modulated by fetal programming, we hypothesized that early-life NMDAR antagonism may affect aspartame-induced glucose deregulation in adulthood, and may alter the aspartame behavioral phenotype.

Prediabetic changes in gene expression induced by aspartame and monosodium glutamate in Trans fat-fed C57Bl/6 J mice.

Background: The human diet has altered markedly during the past four decades, with the introduction of Trans hydrogenated fat, which extended the shelf-life of dietary oils and promoted a dramatic increase in elaidic acid (Trans-18.1) consumption. Food additives such as monosodium glutamate (MSG) and aspartame (ASP) were introduced to increase food palatability and reduce caloric intake.

Interactive effects of neonatal exposure to monosodium glutamate and aspartame on glucose homeostasis.

Background: Recent evidence suggests that the effects of certain food additives may be synergistic or additive. Aspartame (ASP) and Monosodium Glutamate (MSG) are ubiquitous food additives with a common moiety: both contain acidic amino acids which can act as neurotransmitters, interacting with NMDA receptors concentrated in areas of the Central Nervous System regulating energy expenditure and conservation. MSG has been shown to promote a neuroendocrine dysfunction when large quantities are administered to mammals during the neonatal period.

Gender dimorphism in aspartame-induced impairment of spatial cognition and insulin sensitivity.

Previous studies have linked aspartame consumption to impaired retention of learned behavior in rodents. Prenatal exposure to aspartame has also been shown to impair odor-associative learning in guinea pigs; and recently, aspartame-fed hyperlipidemic zebrafish exhibited weight gain, hyperglycemia and acute swimming defects. We therefore investigated the effects of chronic lifetime exposure to aspartame, commencing in utero, on changes in blood glucose parameters, spatial learning and memory in C57BL/6J mice.

Laser biomodulation of normal and neoplastic cells.

This study was designed to determine the laser dose for the stimulation, zero-bioactivation, and inhibition of normal and neoplastic cells in vitro. The medical use of laser biomodulation has been occurring for decades in the area of tissue healing and inflammatory conditions. The potential to modulate the regeneration and differentiation of early cellular precursors by laser photons is a valuable endeavor searching for novel and efficient methods.

Visible lasers were better than invisible lasers in accelerating burn healing on diabetic rats.

Objective: This study was designed to assess and compare the efficacy of accelerating burn healing in diabetic rats using low-power visible and invisible lasers.

Background Data: Low-level laser therapy (LLLT) has been used in a number of diabetic animal and human studies, with both positive and no effects.

Materials And Methods: Male Sprague-Dawley rats were used in the study.

Low-level laser therapy enhances wound healing in diabetic rats: a comparison of different lasers.

Objective: The effects of wound healing acceleration on diabetic rats were determined and compared using different laser wavelengths and incident doses.

Background Data: Many studies have demonstrated that low-level laser therapy (LLLT) can promote the wound healing on non-diabetic animals.

Methods: Male Sprague-Dawley rats were used.

Polychromatic LED in oval full-thickness wound healing in non-diabetic and diabetic rats.

Objective: Our goal was to determine the efficacy of polychromatic light-emitting diode (LED) in the enhancement of wound healing in non-diabetic and diabetic rats.

Background Data: LEDs are increasingly used as an alternative light source for phototherapy.

Methods: A cluster of 25 LED photons at 510-543, 594-599, 626-639, 640-670, and 842-872 nm wavelengths with 272-mW output power was used.

Polychromatic LED therapy in burn healing of non-diabetic and diabetic rats.

Objective: We determined the effect of polychromatic light-emitting diodes (LED) in burn healing of non-diabetic and streptozotocin-induced diabetic rats.

Background Data: LEDs were used as the light source for phototherapy.

Materials And Methods: The polychromatic LED is a cluster of 25 diodes emitting photons at wavelengths of 510-543, 594-599, 626-639, 640-670, and 842-879 nm with 272-mW output power.