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Compositional profiles and mapping of selected mafic microgranular enclaves (MMEs) in Muchen quartz monzonite in eastern South China give constraints on the interaction between mingling mafic and felsic magmas. The intrusion is a typical I-type MME-bearing magnetite-series granitoid in western Pacific. The MMEs and host quartz monzonite are not deformed and have similar magnetic fabrics, which does not support the MMEs are restites or earlier solidified mafic rocks but implies mafic magma globules flowed with felsic magma. The two MMEs represent mafic magma interacting with felsic magma at early and late stage, respectively. The late-stage MME has a Hbl-Bt-Kfs-Pl-Mag assemblage. The early-stage MME has a Cpx-Bt-Kfs-Pl-Mag assemblage with a rim similar to the late-stage MME. Acicular apatite implies rapid cooling of the mafic magmas; however, the similar isotopic ratios and mafic silicate compositions of the MME and quartz monzonite indicate partial equilibrium during magma interactions. Al-in-hornblende estimates the pluton emplacement at ~3.1–3.6 km and therefore the magma mingling-mixing still worked at shallow levels. Most trace element Harker diagrams do not produce linear variation trends and magma mixing cannot solo explain such a pattern. Enrichments of Na2O, REE, Y, Nb, Ta, Ga, Fe3+ and depletions of K2O, Rb, Ba, Sr in the MMEs through diffusion caused noticeable chemical differentiation of both mafic and felsic magmas. Therefore, mass transfer during magma mingling is an important mechanism influencing petrography and chemical compositions of I-type granitoids. Such processes may also extensively occur in the deep hot zones of the continental arc environments.

This paper reviews the technical details of the small diameter sampling method in a study of anisotropy of magnetic susceptibility (AMS) and X-ray CT (computed tomography) and their applications to studies of MMEs (Mafic Microgranular Enclaves) in granite. The AMS results based on 9 mm diameter cylinder specimens collected from the Cretaceous Tongkengxi mafic dykes in South China were consistent with results using 25 mm diameter specimens. The first case study demonstrated the variation of AMS in the interior of a large MME from South China, which contained a center of strong short-range magnetic lineation. This type of magnetic fabric could be detected only by using sample cores with a small diameter. In the foliation direction, the host granite interacted with the MME more heavily and produced a region with a high magnetite content. The second case study was the investigation of the MMEs in the Early Cretaceous Muchen complex in eastern South China. The MME swarms exhibited relatively uniform magnetic fabrics at the outcrop scale, but the fabrics varied significantly at the intrusion scale. AMS of the MME swarms is coaxial with that of the host granite only at some localities. The disagreement of AMS between MME and host granite either imply different magma flow directions, or different magma flow velocities, or disturbance of the granite fabric by the MME. The MMEs in a mylonitic granite from eastern North China were also studied. The MME specimens show highly variable magnetic susceptibility and lineations. They can be only studied appropriately by a small drill. In the three cases, the three magnetic susceptibility axes of the MMEs are consistent with the volume-weighted maximum eigenvector of long/intermediate/short axes of magnetite. The orientations of the magnetite long axes in the three cases form several modes and the concentration of the modes results in a strong lineation. One implication of this study is that MMEs, with the same magmatic fabrics as their host granite, most likely represent mafic magmas flowing with granitic magmas. Another implication is that the interaction between MMEs and host granite, which is strengthened by magmatic flows or ductile deformations, may promote crystallization of magnetite and formation of magnetite-rich granitoids. The presented 9 mm sampling methods provides easy ways to study the petrofabrics and other properties of small-sized features such as MMEs and their detailed internal textures.

Body weight is neither stationary nor does it change unidirectionally. Rather, body weight usually oscillates up and down around a set point. Two types of forces determine the direction of weight changes. Forces that push body weight away from the set point are defined as non-homeostatic and are governed by multiple mechanisms, including, but not limited to, hedonic regulation of food intake. Forces that restore the set point weight are defined as homeostatic, and they operate through mechanisms that regulate short-term energy balance driven by hunger and satiation and long-term energy balance driven by changes in adiposity. In the normal physiological state, the deviation of body weight from the set point is usually small and temporary, and is constantly corrected by homeostatic forces. Metabolic obesity develops when body weight set point is shifted to an abnormally high level and the obese body weight becomes metabolically defended. In hedonic obesity, the obese body weight is maintained by consistent overeating due to impairments in the reward system, although the set point is not elevated. Adaptive increases in energy expenditure are elicited in hedonic obesity because body weight is elevated above the set point. Neither subtype of obesity undergoes spontaneous resolution unless the underlying disorders are corrected. In this review, the need for both appropriate patient stratification and tailored treatments is discussed in the context of the new framework of metabolic and hedonic obesity.

The gut is responsible for food intake, which, together with energy expenditure, determines the status of energy balance. Positive net caloric intake directly correlates with the size of fat tissue weight gain. The gut fulfills the function of regulating food intake by communicating with other organ systems, particularly the brain, to control meal content, frequency, and size. While it receives efferent output from the brain to signal hunger, satiation, or general “appetite” based on the body’s metabolic and hedonic needs, it sends afferent signals to inform the brain the status of food intake, completing a negative feedback loop. Broadly speaking, the gut has “taste receptors” throughout the intestine, in addition to the traditional taste buds in the mouth. While the bolus of food ingested is sensed by mechanosensors in the gut, the nutrients derived from ingested foods are sensed by chemosensors, which leads to the secretion of many peptide hormones by the enteroendocrine cells. These gut hormones may communicate with the brain directly via endocrine action, or indirectly through vagal afferent neurons, to exert their orexigenic or anorexigenic effects. This chapter summarizes major gut hormones related to energy metabolism, their roles in regulating appetite and food intake, and where evidence calls for, their roles in long-term energy balance, usually in concert with signals from adipose tissue and with nonhomeostatic signals. The roles of bile acids and gut microbiota and their interplays with the gut hormones and other organ systems involved in energy metabolism are also briefly discussed.

Body weight is neither stationary nor does it change unidirectionally. Rather, body weight usually oscillates up and down around a set point. Two types of forces determine the direction of weight changes. Forces that push body weight away from the set point are defined as non-homeostatic and are governed by multiple mechanisms, including, but not limited to, hedonic regulation of food intake. Forces that restore the set point weight are defined as homeostatic, and they operate through mechanisms that regulate short-term energy balance driven by hunger and satiation and long-term energy balance driven by changes in adiposity. In the normal physiological state, the deviation of body weight from the set point is usually small and temporary, and is constantly corrected by homeostatic forces. Metabolic obesity develops when body weight set point is shifted to an abnormally high level and the obese body weight becomes metabolically defended. In hedonic obesity, the obese body weight is maintained by consistent overeating due to impairments in the reward system, although the set point is not elevated. Adaptive increases in energy expenditure are elicited in hedonic obesity because body weight is elevated above the set point. Neither subtype of obesity undergoes spontaneous resolution unless the underlying disorders are corrected. In this review, the need for both appropriate patient stratification and tailored treatments is discussed in the context of the new framework of metabolic and hedonic obesity.