Gender-associated differences in oral microbiota and salivary biochemical parameters in response to feeding.

Saliva plays a key role in food absorption and digestion mainly due to both its enzymes and microbiota. The main objective of this study was to compare the oral microbiota and salivary parameters between men and women in response to feeding. To answer this question, we set up a pilot study on 10 male and 10 female subjects to examine the role of saliva in glycaemia physiology. Biological parameters and the microbiotal composition of saliva were analyzed in fasted and fed states. The results show that the level of blood glucose was not different between men and women in the fasted state (88.00 mg/dL ± 6.38 vs 87.00 mg/dL ±8.07, p = 0.9149) or in the fed state (102.44 mg/dL ± 14.03 vs 116.9 mg/dL ± 25, p = 0.1362). Free fatty acids (FFA 0.15 mmol/L ± 0.15 vs 0.07 mmol/L ± 0.07, p = 0,0078), cholesterol (0.53 mmol/L ± 0.30 vs 0.15 mmol/L ± 0.14, p < 0.0001), and total saliva proteins (13.2 g/L ± 4.31 vs 9.02 g/L ± 6.98, p = 0.0168) were decreased after feeding, as well as the saliva lipase (27.89 U/L ± 25.7 vs 12.28 U/L ± 4.85, p = 0.0126). A very significant increase in the relative abundance of Streptococcaceae (24.56 ± 9.32 vs 13.53 ± 7.47, p = 0.00055) and a decrease in Prevotellaceae (34.45 ± 9.30 vs 17.43 ± 9.03, p = 0.00055) were observed in the fed condition. When investigating gender-related differences in the fasted state, men showed higher levels of cholesterol (0.71 mmol/L ± 0.26 vs 0.40 mmol/L ± 0.27, p = 0.0329), FFA (0.25 mmol/L ± 0.18 vs 0.08 mmol/L ± 0.06, p = 0.0049), and triglycerides (0.24 mmol/L ± 0.15 vs 0.09 mmol/L ± 0.04, p = 0.006) than women. Finally, differences could be observed in saliva microbiota between men and women in the fasted condition but even more in the fed condition, where Porphyromonas and Capnocytophaga were overrepresented in the male salivary samples compared with female saliva. Thus, biological parameters and microbiota in saliva could be the signatures of the feeding conditions and sex gender status.

Young microbes for adult obesity.

Gut microbes are active participants of host metabolism. At birth, child physiology is committed towards healthiness or sickness depending, in part, on maternal condition (i.e. lean vs obesity) and delivery. Finally, changes from breastfeeding to solid food also account to define gut microbiota ecology in adulthood. Nowadays, alterations of gut microbiota, named dysbiosis, are acquired risk factors for multiple diseases, especially type 2 diabetes and obesity. Despite important evidence linking nutrition to dysbiosis to energetic dysmetabolism, molecular mechanisms for causality are still missing. That the status of gut microbiota of mother and child is crucial for future diseases is witnessed by adulthood overweight and obesity observed in children with dysbiosis. In this short review we highlight the importance of early life events related to the microbiota and their impact on future adult disease risk. Therefore, our effort to treat or prevent metabolic diseases should be addressed towards early or previous life steps, when microbial decisions are going to affect our metabolic fate.

Managing the manager: gut microbes, stem cells and metabolism.

One major discovery of the last decade in the field of metabolic diseases is that the microorganisms comprising the gut microbiota are now considered a metabolic "organ", modulating multiple functions of the host, such as intestinal immune system maturation, adiposity, cardiac metabolism, liver triglyceride storage, and brain development and behaviour. The corresponding mechanisms involve increased energy harvesting through the production by microbiota of short-chain fatty acids for use by the host, and the release of pro-inflammatory compounds, such as lipopolysaccharide (LPS), flagellin and peptidoglycan. In particular, a high-fat diet (HFD) modifies gut microbiota, resulting in an increase of plasma LPS levels known as "metabolic endotoxaemia", a major driver of the onset of metabolic diseases through a CD14-dependent mechanism. The LPS-sensitive cell types can be seen within bone marrow-derived cells (BMC), which are involved in the development of inflammation in the adipose tissue of obese and type 2 diabetic mice. Furthermore, the expression of LPS receptor/cofactor CD14 cells from the stromal vascular fraction of adipose depots can also be directly targeted by LPS to initiate precursor cell development and adiposity. Moreover, data from the literature also indicate an impact of gut microbiota on intestinal stem cells. Thus, this mini review presents the experimental evidence supporting a relationship between gut microbiota and stem cells as a new axis of metabolic homoeostasis control.

[Metabolic therapy at the edge between human hosts and gut microbes]. / La thérapie métabolique à l'interface entre l'homme et le microbiote intestinal.

Personalized medicine is becoming day-after-day more urgent taking into account the great diversity characterizing patients affected by a given pathology, especially metabolic diseases. In fact, antidiabetic/obesity treatments have shown a reduced or no effect at all in some patients, representing a major challenge physicians have to face worldwide. Therefore, efforts have to be put to identify individual factors affecting our susceptibility towards a given medication. In that regard, gut microbiota may stand for the missing piece of the metabolic puzzle regulating host response, since its role in the induction of metabolic diseases has now been achieved. In fact, we firstly provided a bacterial explanation for the low-grade chronic inflammation featuring metabolic diseases, by showing the lipopolysaccharide as a trigger and risk factor of such pathologies. However, despite similar lineages of microbes characterize the gut of people, important differences still remain, which may be responsible for opposite effect of treatments such as pre- or probiotics, whose efficacy seems to be governed by the own gut microbiota of subjects. We have recently shown that gut microbiota is associated to the inclination to resist or not high-fat diet-induced type 2 diabetes in mice. In addition, the direct targeting of gut microbes by dietary fibers reversed the observed metabolic phenotype. These results, together with the literature, strongly suggest gut microbiota as a new target for the development of personalized metabolic therapy.

[Impact of periodontal disease on arterial pressure in diabetic mice]. / Impact de la maladie parodontale sur la pression artérielle des souris diabétiques.

Diabetes-driven cardiovascular diseases represent a high challenge for developed countries. Periodontal disease is strictly linked to the aforementioned diseases, due to its Gram negative-driven inflammation. Thus, we investigated the effects of periodontal disease on arterial pressure during the development of diabetes in mice. To this aim, C57BL/6 female mice were colonized with pathogens of periodontal tissue (Porphyromonas gingivalis, Prevotella intermedia and Fusobacterium nucleatum) for 1month, whereas another group of mice did not undergo the colonization. Subsequently, all mice were fed a high-fat carbohydrate-free diet for 3months. Then, arterial pressure was measured in vivo and a tomodensitometric analysis of mandibles was realized as well. Our results show increased mandibular bone-loss induced by colonization with periopathogens. In addition, periodontal infection augmented glucose-intolerance and systolic and diastolic arterial pressure, parameters already known to be affected by a fat-diet. In conclusion, we show here that periodontal disease amplifies metabolic troubles and deregulates arterial pressure, emerging as a new axis of metabolic investigation.