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Diet as a Potential Modulator of Body Fat Distribution
Published in Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss, Nutrition and Cardiometabolic Health, 2017
Sofia Laforest, Geneviève B. Marchand, André Tchernof, Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss
Medium-chain triglycerides (MCT) have unique properties that distinguish them from long-chain triglycerides (LCT). These characteristics seem to confer beneficial metabolic effects. MCT, after cleavage to glycerol and FA, are transported directly to the liver by the portal vein, bypassing incorporation into chylomicrons and the lymphatic system (Poppitt et al. 2010). Unlike LCT, the MCT do not require the carnitine acyltransferase enzyme to be incorporated into the mitochondria, allowing more rapid β-oxidation, a phenomenon that has been linked with greater energy expenditure and less weight gain (Bach and Babayan 1982). MCT may also increase satiety after a meal (Van Wymelbeke et al. 1998, Krotkiewski 2001, Poppitt et al. 2010). Generally, MCT comprise FA from 6 to 10 and even 12 carbons, since lauric acid (C12:0), structurally classified as an LCT, shows properties that are similar to caprylic (C8:0) and capric (C10:0) acids. MCT are found primarily in vegetable oils such as coconut (71%) and palm kernel (48%) (Health Canada 2010).
Nutrient Interactions and Glucose Homeostasis
Published in Emmanuel C. Opara, Sam Dagogo-Jack, Nutrition and Diabetes, 2019
One strategy that has received significant attention is the use of fatty acid oxidation inhibitors in the management of type 2 diabetes. As can be predicted from the glucose-fatty acid cycle, the rationale in the use of this approach is that inhibiting fatty acid oxidation would enhance peripheral tissue glucose utilization, while inhibiting gluconeogenesis. Hence, there has been significant interest in the development of drugs to inhibit fatty acid oxidation and improve glycemic control in individuals with type 2 diabetes. Long-chain fatty acids are converted to fatty acyl-CoA esters in the outer mitochondrial membrane and require carnitine to get across the inner mitochondrial membrane for oxidation in the mitochondrial matrix. The rate-limiting enzyme that catalyzes the transesterification of the fatty acyl group from Co-A to carnitine is carnitine acyltransferase 1, the predominant form being the carnitine palmitoyl transferase 1 (CPT-1). It is therefore not surprising that the first generation of fatty acid oxidation inhibitors developed as therapeutic agents for type 2 diabetes were inhibitors of the CPT-1 enzyme [36,38]. CPT-1 inhibitors like etomoxir and tetradecylglycidic acid (TDGA), have the ability to decrease blood glucose levels. However, enthusiasm for the use of this class of inhibitors of fatty acid oxidation waned because of observations that they induced cardiac hypertrophy in rodents treated with the drugs. The next generation of CPT-1 inhibitors developed were drugs, such as SDZ and CPI 975, whose action on the liver-specific enzyme is reversible and might therefore be less toxic to the heart. Also, some monoamine oxidase inhibitors have been shown to inhibit the acylcarnitine translocase/CPT-2 enzyme and cause reductions in blood glucose levels [38]. Further studies are required to assess both the long-term efficacy and safety of these newer compounds in human subjects.
Nutrient Interactions and Glucose Homeostasis
Published in Emmanuel Opara, NUTRITION and DIABETES, 2005
One strategy that has received significant attention is the use of fatty-acid oxidation inhibitors in the management of type 2 diabetes. As can be predicted from the glucose–fatty-acid cycle, the rationale in the use of this approach is that inhibiting fatty-acid oxidation would enhance peripheral tissue glucose utilization while inhibiting gluconeogenesis. Hence, there has been significant interest in the development of drugs to inhibit fatty-acid oxidation and improve glycemic control in individuals afflicted with type 2 diabetes. Long-chain fatty acids are converted to fatty acyl-CoA esters in the outer mitochondrial membrane and require carnitine to get across the inner mitochondrial membrane for oxidation in the mitochondrial matrix. The rate-limiting enzyme that catalyzes the transesterification of the fatty acyl group from Co-A to carnitine is carnitine acyltransferase 1, the predominant form being the carnitine palmitoyl transferase 1 (CPT-1). It is therefore not surprising that the first generation of fatty-acid oxidation inhibitors developed as therapeutic agents for type 2 diabetes were inhibitors of the CPT-1 enzyme (19, 21). CPT-1 inhibitors, such as etomoxir and tetradecylglycidic acid (TDGA), have the ability to decrease blood-glucose levels. However, enthusiasm for the use of this class of inhibitors of fatty-acid oxidation waned because of observations that they induced cardiac hypertrophy in rodents treated with the drugs. The next generation of CPT-1 inhibitors developed were drugs, such as SDZ and CPI 975, whose action on the liver-specific enzyme is reversible and might therefore be less toxic to the heart. Also, some monoamine oxidase inhibitors have been shown to inhibit the acylcarnitine translocase/CPT-2 enzyme and cause reductions in blood-glucose levels (21). Further studies are required to assess both the long-term efficacy and safety of these newer compounds in human subjects.
Intake of Diacylglycerols and the Fasting Insulin and Glucose Concentrations: A Meta-Analysis of 5 Randomized Controlled Studies
Published in Journal of the American College of Nutrition, 2018
Xu Tongcheng, Jia Min, Li Xia, Qiu Bin, Zhang Yuan, Liu Wei, Zong Aizhen, Liu Lina, Du Fangling
The structural difference of TAG and DAG leads to their different metabolic processes. In general, TAG is hydrolyzed by 1,3-lipase, generating 1,2-DAG or 2,3-DAG, which can be further metabolized to 2-monoacylglycerol (MAG) and FAs, whereafter, 2-MAG and FAs can be absorbed into intestinal epithelial cells where the hydrolysates re-esterified to chylomicron-TAG. On the other side, DAG is hydrolyzed to 1-MAG and can be further metabolized to glycerol and FAs, which are less likely resynthesized to chylomicron-TAG, since the affinities of 1-MAG or 3-MAG for MAG acyltransferase (MGAT) in epithelial cells are lower than that of 2-MAG for MGAT (1). As a result, DAG releases more FAs, which are transported to liver for β-oxidation (2). The enhancement of β-oxidation caused by DAG is proved by many experiments. Meng et al. (26) measured the activity of acyl-CoA carnitine acyltransferase (ACAT) and acyl-CoA DAG acyltransferase (DGAT), which are the key enzyme of β-oxidation and the acylation enzyme of DAG to TAG, respectively. The experiment found that DAG up-regulates ACAT and down-regulates DGAT, indicating that DAG stimulates β-oxidation and represses anabolism of TAG (1). In a respiratory gas measurement experiment conducted by Kamphuis et al. (27) fat oxidation calculated from DAG oil diet was highly increased compared with TAG oil (10–24).
Associations between ketone bodies and fasting plasma glucose in individuals with post-pancreatitis prediabetes
Published in Archives of Physiology and Biochemistry, 2020
Sakina H. Bharmal, Sayali A. Pendharkar, Ruma G. Singh, David Cameron-Smith, Maxim S. Petrov
One mechanism could be the suppression of lipolysis by insulin, leading to a reduced availability of fatty acid substrates for ketogenesis. However, in individuals with dysregulated glucose homeostasis after AP, increased circulating levels of glycerol are suggestive of an upregulation of lipolysis (Gillies et al. 2017). That study also showed that there was no significant change in free fatty acid levels. These findings suggest that fatty acids are channelled towards re-esterification rather than ketogenesis, in the hyperinsulinaemic setting of PPP. Insulin stimulates the activity of enzyme acetyl-CoA carboxylase, which catalyses the formation of malonyl-CoA. Increase in the concentrations of malonyl-CoA inhibits carnitine acyltransferase 1, further inhibiting the entry of fatty acids into the mitochondria for oxidation to ketones (McGarry and Foster 1980, Johnston and Alberti 1982). These fatty acids could be shunted to triglyceride synthesis, as noted by increased serum triglyceride levels in individuals with altered glucose homeostasis after AP (Gillies et al.2017). The suppressive action of insulin is further supported by several significant associations between ketone bodies and indices of insulin resistance. In the present study, BHB was significantly inversely associated with adipose tissue-specific insulin resistance (as determined by Adipo-IR and IG indices), as well as general insulin resistance (as determined by HOMA-IR). β-hydroxybutyrate decreased by 0.10 mmol/L (p <.001) with every unit change in Adipo-IR and by 0.16 mmol/L (p = .007) with every unit change in IG index, in individuals with PPP. From these findings, it appears that, in the presence of hyperinsulinaemia, ketogenesis is suppressed, which favours a lipogenic profile in the post-pancreatitis setting. The other mechanism could be insulin’s effect on ketolysis. Several clinical studies have demonstrated peripheral utilisation of ketone bodies (in particular, BHB) to be linked to insulin concentrations (Hall et al.1984, Nosadini et al.1985, Keller et al.1988). Although we did not measure insulin’s effect on ketolysis, based on previous evidence it can be suggested that high circulating levels of insulin stimulate the extra-hepatic organs to metabolise BHB in order to generate energy. However, the exact mechanisms underlying utilisation of ketone bodies in PPP remain to be investigated.