Lately, the incidence of overweight, obesity, and type 2 diabetes has shown a staggering increase. To prevent and treat these conditions, one must look at their etiology. As life on earth has evolved under the conditions of nature’s 24‐hour light/dark cycle, it seems likely that exposure to artificial light at night (LAN) would affect physiology. Indeed, ample evidence has shown that LAN impacts many metabolic parameters, at least partly via the biological clock in the suprachiasmatic nucleus of the hypothalamus. This review focuses on the impact of chronic and acute effects of LAN of different wavelengths on locomotor activity, food intake, the sleep/wake cycle, body temperature, melatonin, glucocorticoids, and glucose and lipid metabolism. While chronic LAN disturbs daily rhythms in these parameters, experiments using short‐term LAN exposure also have shown acute negative effects in metabolically active peripheral tissues. Experiments using LAN of different wavelengths not only have indicated an important role for melanopsin, the photopigment found in intrinsically photosensitive retinal ganglion cells, but also provided evidence that each wavelength may have a specific impact on energy metabolism. Importantly, exposure to LAN has been shown to impact glucose homeostasis also in humans and to be associated with an increased incidence of overweight, obesity, and atherosclerosis.

In our modern society, the exposure to light at night (LAN) has increased considerably, which may impact human health negatively. Especially exposure to light at night containing short wavelength emissions (~450–500 nm) can disrupt the normal function of the biological clock, altering sleep‐wake cycles and inducing metabolic changes. Recently, we reported that light at night acutely impairs glucose tolerance in nocturnal rats. However, light at night in nocturnal rodents coincides with their activity period, in contrast to artificial light at night exposure in humans. The aim of this study was to evaluate the acute effects of blue (λ = 490 ± 20 nm) artificial light at night (bALAN) on glucose metabolism and food intake in both male and female diurnal Sudanian grass rats (Arvicanthis ansorgei) fed either regular chow or a free choice high‐fat high sucrose diet (HFHS). In both chow and HFHS fed male Arvicanthis, 1‐hour of bALAN exposure induced a higher glucose response in the oral glucose tolerance test (OGTT) accompanied by a significant decrease in plasma insulin. Furthermore, in HFHS fed animals, bALAN induced an increase in sucrose intake during the dark phase in males but not in females. Additionally, 1‐h of bALAN increased the nonfasted glucose levels together with plasma corticosterone in female grass rats. These results provide new and further evidence for the deleterious effects of exposure to short wavelength emission‐containing artificial light at night on glucose metabolism in a diurnal rodent in a sex‐dependent manner.

Objective Intrinsically photosensitive retinal ganglion cells are most sensitive to short wavelengths and reach brain regions that modulate biological rhythms and energy metabolism. The increased exposure nowadays to artificial light at night (ALAN), especially short wavelengths, perturbs our synchronization with the 24‐hour solar cycle. Here, the time‐ and wavelength dependence of the metabolic effects of ALAN are investigated. Methods Male Wistar rats were exposed to white, blue, or green light at different time points during the dark phase. Locomotor activity, energy expenditure, respiratory exchange ratio (RER), and food intake were recorded. Brains, livers, and blood were collected. Results All wavelengths decreased locomotor activity regardless of time of exposure, but changes in energy expenditure were dependent on the time of exposure. Blue and green light reduced RER at Zeitgeber time 16‐18 without changing food intake. Blue light increased period 1 ( Per1) gene expression in the liver, while green and white light increased Per2 . Blue light decreased plasma glucose and phosphoenolpyruvate carboxykinase ( Pepck) expression in the liver. All wavelengths increased c‐Fos activity in the suprachiasmatic nucleus, but blue and green light decreased c‐Fos activity in the paraventricular nucleus. Conclusions ALAN affects locomotor activity, energy expenditure, RER, hypothalamic c‐Fos expression, and expression of clock and metabolic genes in the liver depending on the time of day and wavelength.

Objectives: We have previously shown that the combined consumption of fat and a sucrose solution induces overeating, and there is evidence indicating that sucrose drinking directly stimulates fat intake. One neurochemical pathway by which sucrose may enhance fat intake is through the release of endogenous opioids in the nucleus accumbens (NAC). Methods: To test this hypothesis, we provided rats with a free-choice high-fat diet for two weeks. During the second week, rats had access to an additional bottle of water or a 30% sucrose solution for five minutes per day. After these two weeks, we infused vehicle or the μ-opioid receptor agonist [D-Ala2, N-MePhe4, Gly-ol]-enkephalin (DAMGO) into the NAC 30 min after their daily access to the additional bottle of water or the sucrose solution. Results: Sucrose drinking had two effects, (1) it stimulated fat intake in the absence of DAMGO infusion, (2) it diminished sensitivity to DAMGO, as it prevented the rapid increase in fat intake typically seen upon DAMGO infusion in the nucleus accumbens. In a second experiment, we confirmed that these results are not due to the ingested calories of the sucrose solution. Lastly, we investigated which brain areas are involved in the observed effects on fat intake by assessing c-Fos-expression in brain areas previously linked to DAMGO's effects on food intake. Both intra-NAC DAMGO infusion and sucrose consumption in the absence of DAMGO infusion had no effect on c-Fos-expression in orexin neurons and the central amygdala but increased c-Fos-expression in the NAC as well as the basolateral amygdala. Discussion: In conclusion, we confirm that sucrose drinking stimulates fat intake, likely through the release of endogenous opioids.