Carbohydrates are a key source of energy for insects. Carbohydrates, mainly in the form of glycogen, trehalose and glucose, play an important role in energy metabolism and metabolite synthesis (Gaxiola et al., 2005; Kehl and Fischer, 2012). They not only enhance insect hunger resistance, but also play a vital role in other physiological adaptations (Tang et al., 2012b; Chng et al., 2017). Studies have found that starved larvae of A. mellifera can still maintain a stable blood sugar trehalose concentration (Wang et al., 2016a).

When the blood sugar content of insects is low, glycogen can be broken down, especially during starvation (Marron et al., 2003; Arrese and Soulages, 2010; Parkash et al., 2012; Tang et al., 2012a; Rovenko et al., 2015). Glucose is an equally important carbohydrate and all sugars are eventually converted to glucose to provide ATP, an energy source and metabolic intermediate in living cells (Jensen et al., 2015). Trehalose, an important component of insect blood is also known as the “sugar of life” (Shukla et al., 2015). In harsh environments, such as severe cold, high temperature and drought, trehalose accumulates and is used to maintain normal life processes and enhanced survival (Yu et al., 2008). Glycogen, glucose and trehalose can be converted into other forms for energy storage and release in insects (Tang et al., 2010). When insects are starved, trehalose is used first as a source of energy (Tang et al., 2014), leading to a rapid decrease in glucose and trehalose in their hemolymph (Satake et al., 2000). Under starvation stress, the trehalose content of Trogoderma granarium larvae was significantly reduced (Mohammadzadeh and Izadi, 2018). In starved P. hilaris larvae, glucose levels significantly decreased and the level of trehalose showed an initial decrease, followed by an increase (Munyiri and Ishikawa, 2005). The hunger-tolerance mechanisms of insects differ. For example, the hemolymph glucose concentration of A. mellifera was significantly reduced under starvation stress (Buckemüller et al., 2017) whereas the phosphorylase activity of Bombyx mori and Manduca sexta larvae increased and the glycogen content gradually decreased (Meyer-Fernandes et al., 2000; Satake et al., 2000). When the intensity of starvation stress increases, glycogen is converted to trehalose and released into the blood to maintain energy metabolism (Bede et al., 2007). Therefore, as the intensity of starvation increases, the levels of trehalose and glycogen in insects decrease, but trehalose remains at a relatively low and stable concentration (Shi et al., 2017). After relief from hunger stress, the hemolymph glucose levels of insects increase (Sánchez-Paz et al., 2007) and are gradually converted into trehalose and glycogen for storage.

The most important substances that mediate the decomposition of carbohydrates are trehalose synthase (TPS), trehalase (TREH), glycogen synthase (GS), and insulin-like pathway-related genes (Tang et al., 2012b). In H. axyridis exposed to starvation stress, the trehalose level and trehalase activity were significantly lower 8 h after starvation treatment, but the relative expression of TRE1-1 increased. After 8–24 h of starvation, trehalose was maintained at a high level, but glycogen levels decreased. These results indicate that trehalose plays a key role in the starvation process through molecular and biochemical regulation of trehalose and glycogen metabolism (Tang et al., 2014; Shi et al., 2017). When human blood sugar levels are very low, the body increases the blood sugar concentration by regulating the insulin signaling pathway. For insects, insulin-like signaling pathways in vivo play a similar role in controlling the balance of blood glucose concentrations (Kuhn et al., 2015; Zhai et al., 2015). Similarly, in D. melanogaster and B. mori, a decrease in insulin-like signaling levels regulate the expression of related antimicrobial peptide genes (Becker et al., 2010; Yang et al., 2016; Lebreton et al., 2017). These genes participate in immune regulation and repair of damage and thereby enhance the resistance of insects to starvation (Riddell and Mallon, 2006).

Fat bodies are the main units of lipid storage in insects and their storage function is key for normal life processes (Ballard et al., 2008; Kehl and Fischer, 2012; Park et al., 2013). To combat hunger, stored lipid resources are often used through reduced glucose oxidation and increased fatty acid mobilization and lipid oxidation (Gergs and Jager, 2014; McCue et al., 2015; Wang et al., 2016a). Lipid metabolism in insects is mainly regulated by Adipokinetic hormone (AKH), the fat stimulating hormone, which is secreted under low nutrient conditions, thereby leading to lipolysis, glycogenolysis, and sugar and lipid nutrients moving from the fat body into the hemolymph (Kim and Rulifson, 2004; Lee and Park, 2004). AKH, a key regulator of energy—also mobilizes sugar and lipids from insect fat bodies during high-energy activities such as flight and exercise and contributes to the balance of hemolymph sugars, lipids, and carbohydrates (Staubli et al., 2002; Hou et al., 2017). Intensive research has found that the ability of insects to survive starvation is largely dependent on the ratio of triglycerides to lipids in the body (Renault et al., 2002; Ballard et al., 2008; Laparie et al., 2012). When insects fly under starvation conditions, lipids are the main source of energy for the flight muscles (Ryan and van der Horst, 2000). Lipids are, therefore, closely linked to insect movement during starvation. Of course, the use of lipids under starvation stress varies among different insects. Under laboratory starvation conditions, the concentration of lipids in the hemolymph of B. mori increased (Satake et al., 2000) whereas in Pachnoda sinuata (Coleoptera: Scarabaeidae), the lipids in the flight muscles and fat bodies significantly decreased (Auerswald and Gäde, 2000). The beetle Merizodus soledadinus (Coleoptera: Carabidae) significantly increased the hydrolysis of triglycerides during food deprivation which returned to normal levels after feeding (Laparie et al., 2012). This suggests that triglycerides are immediately mobilized to enhance hunger resistance in the event of food shortage.

It is worth noting that moderate hunger leads to the accumulation of fat, which is dependent on the developmental stage of the insect and the state of feeding (Lorenz, 2001). Increased fat mass in insects can increase resistance to hunger, indicating a significant correlation between lipid levels and hunger resistance (Parkash et al., 2014). Pure lipid-based triglycerides are used during starvation (Sinclair et al., 2011) and proteins that are starved by lipid synthesis or degradation are affected by the opposite form. For example, a fatty acid synthase and a glycocholine transfer protein were down-regulated four fold after 4 h of starvation, while triacylglycerol lipase levels increased 10 fold (Muhlia-Almazán et al., 2005).

A modest decrease in protein content during insect starvation indicates that insects can cope with hunger by using different endogenous reserves (Gäde and Auerswald, 2002; Helland et al., 2003). After starvation, the concentrations of alanine in the flight muscles, lipid bodies, and hemolymph of insects rapidly decline whereas those of proline remain high (Kehl and Fischer, 2012). At the same time, the heat shock proteins 70 (HSP70s) are important stress protectants in H. axyridis and Rhodnius prolixus (Hemiptera, Reduviidae) and play a role in adaptation to food deprivation (Shen et al., 2015; Paim et al., 2016). In addition, studies have shown that the positive effects of adult amino acids are limited to females, presumably because their high protein demand significantly changes the catabolic rate (Mevi-Schütz and Erhardt, 2005; Bauerfeind and Fischer, 2009). There is ample evidence that amino acids extracted from protein breakdown are degraded during starvation (Haubert et al., 2005).

When insects are stressed by hunger, they initiate a series of anti-starvation mechanisms. These mechanisms include regulating the expression of related genes, synthesizing anti-stress substances and regulating the catabolism of energy substances in the body to maintain normal growth and development (Buckemüller et al., 2017). A study in D. melanogaster found that dG9a (histone methyltransferase) is a key factor in tolerance to hunger stress and is also a key regulator of behavioral strategies under starvation conditions (An P.N.T. et al., 2017; Shimaji et al., 2017). Hunger is a powerful driver of food intake and some neurons, neuropeptides and neurohormones play key roles in behavioral and physiological regulation (Perić-Mataruga, 2006; Jourjine et al., 2016; Mena et al., 2016). At the same time, starvation increases the expression level of SLC5A11 neurons and enhances their excitability by inhibiting the dKCNQ channel, thereby conferring hunger status and promoting feeding and starvation-driven behaviors (Park et al., 2016).

Hunger itself affects stress in insects and the expression of immunity-related genes. Many immunity-related genes, such as interleukin 1-β, are significantly down-regulated during starvation (Riddell and Mallon, 2006; Buckemüller et al., 2017) leading to lower metabolism followed by a concomitant decline in immunity (Guo et al., 2014). Starvation stress can also significantly up-regulate the expression of two octopamine (OA) receptor genes (Li, 2017). OA has significant biological effects on the growth and behavior of various arthropods and poor living conditions pose differential consequences on the distribution and content of OA. Hunger not only has an effect on the transcription of the brain and surrounding tissues in Drosophila (Bos et al., 2016; Singh et al., 2018), but also induces autophagy in Drosophila larvae during metamorphosis by inhibiting the PI3KI/Akt-Tor pathway (Riddiford et al., 2000; Wang et al., 2012). Similarly, starvation can also induce autophagy in Spodoptera frugiperda (Lepidoptera: Noctuidae) Sf9 cells (Xie K. et al., 2017). Increased levels of autophagy are usually induced by signals such as starvation, while excessive levels of autophagy can cause autophagic programmed cell death. During starvation, the level of autophagy helps to reduce the level of apoptosis in fat cells, thus playing a protective role in the survival of adipocytes (Otomo et al., 2013; Li et al., 2015).

Dopaminergic signaling pathways and juvenile hormones (JH) are also important stress-resistance substances in insects and play a role in adaptation to hunger stress (Neckameyer and Weinstein, 2005; Lee and Horodyski, 2006). While the former directly affects the metamorphosis and development of insects (Yang, 2014), the latter confers damage protecting (Shi et al., 2016). After starvation treatment, the growth and development of Plutella xylostella (Lepidoptera: Plutellidae) were found to be delayed because the expression of the juvenile hormone acid methyl transferase (JHAMT) candidate gene Px009591 increased and the expression of the juvenile hormone esterase (JHE) gene Px004817 and JHE activity decreased. These changes led to an increase in JH levels in insects, which in turn delayed growth and development (Duan, 2016). Similarly, the rate of biosynthesis of M. sexta gradually increased after starvation (Lee and Horodyski, 2006). Telang et al. (2010) also found that JHE mRNA levels in the 4^th instar larvae of Aedes aegypti (Diptera: Culicidae) were close to zero after 36 h of starvation. In addition, when the expression of the hsp18.3 gene of Tribolium castaneum (Coleoptera: Tenebrionidae) was silenced by RNAi technology, the resistance of the starved group was significantly lower than that of the control group (Xie J. et al., 2017). Similarly, a study of three HSP70 genes in H. axyridis showed that their relative expression not only increased with increasing temperature, but also at the peak of starvation at 8 h (Shen et al., 2015). Thus, juvenile hormones and heat shock proteins have a significant effect on insect emergency stress responses.