Pre-diabetes is a stage that usually precedes the onset of type 2 diabetes with a slight
increase in fasting glucose, between 5.6 and 6.9 mmol/L; decreased glucose tolerance,
between 7.8 and 11 mmol/L; and glycated hemoglobin, between 5.5 and 6.4%
(ADA 2020). These biochemical abnormalities are usually caused by defects in
insulin secretion from pancreatic cells, low insulin activity, or both (Unwin et al.
2002). Pre-diabetes can eventually lead to type 2 diabetes, which is characterized by
hyperglycemia due to the inability of cells to respond fully to insulin, or to be
resistant to insulin. Insulin resistance is characterized by insulin inefficiency in
promoting glucose uptake by tissues and low intracellular glucose concentration
signals for increased insulin production by the pancreas. Over time, depleted pancreatic
beta cells reduce or stop insulin production, further elevating blood glucose
levels (>6.9 mmol/L), characteristic of the diabetes condition. According to epidemiological
data, type 2 diabetes is common in the elderly, but its frequency has
increased in children and young adults due to high rates of obesity, sedentary
lifestyle, and unbalanced diet, with excess fat and sugar. All of these factors indicate
that both type 1 and type 2 diabetes result from a combination of genetic predisposition
and environmental triggers (IDF 2020).
Type 2 diabetes symptoms are similar to those of type 1 diabetes, but they are
difficult to be identified in the early stages due to the long pre-diagnosis process, and,
therefore, up to one third of the population may not be diagnosed early (Bansal 2015;
Kaur 2014; Buchanan et al. 2002). This can be detrimental for a favorable prognosis
after a long period of latent disease, and complications such as retinopathy or ulcers
in the lower limbs that do not heal may occur (Chiasson et al. 2002). Furthermore,visceral obesity common in overweight and obese patients is related to the local and
systemic inflammatory process, closely linked to the development of these
comorbidities (ADA 2020). Regarding the healthy population, individuals with
pre-diabetes and diabetes have a higher risk over the time of developing cardiovascular
disease, metabolic syndrome, and polycystic ovaries, in addition to higher
morbidity and mortality rates (Bansal 2015; Kaur 2014).
Considering the close relationship between pre-diabetes, obesity, and diet, it is
important to examine the influence of intestinal microbiota in this context. Intestinal
microbiota is characterized by a diverse community of bacteria responsible for
influencing nutrient metabolism, immune responses, and resistance to infectious
pathogens (Nicholson et al. 2012; Belkaid and Hand 2014; van Nood et al. 2013).
In the diabetic population, the intestinal microbiota presents a pattern of dysbiosis,
which can be the starting point for the evolution of pre-diabetes to type 2 diabetes
and other chronic diseases (Pratley 2013; Ziemer et al. 2008; Tsui et al. 2008;
Stefanakia et al. 2018). Current scientific evidence has shown that probiotics or
prebiotics, including phenolic compounds, can play a widely recognized role in the
regulation of the intestinal microbiota, altering microbial composition and the
metabolism of the bacteria and host (Tsai et al. 2019; Wang et al. 2020). Based on
these fundamentals, this chapter will address the intrinsic relationships between the
consumption of probiotics and prebiotics in individuals with pre-diabetes and type
2 diabetes.