Estimating Triglyceride Levels Using Total Cholesterol, Low-Density Lipoprotein Cholesterol, and High-Density Lipoprotein Cholesterol Levels: A Cross-Sectional Study.

Objective: Triglyceride (TG) levels are affected by food intake, and the cutoff values for nonfasting TG levels vary. This study aimed to calculate fasting TG levels based on total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) levels. Methods: Multiple regression analysis was performed to determine estimated triglyceride (eTG) levels using data from 39,971 participants divided into six groups based on non-high-density lipoprotein cholesterol (nHDL-C) levels (<100, <130, <160, <190, <220, and ≥220 mg/dL). Results: Provided that fasting TG and eTG levels ≥150 mg/dL were positive and those <150 mg/dL were negative, the three groups (nHDL-C levels <100, <130, and <160 mg/dL) consisting of 28,616 participants had a false-positive rate of <5%. The coefficient and constant terms in the formula for the eTG in groups with nHDL-C levels <100, <130, and <160 mg/dL were as follows: constant terms, 12.193, 0.741, and -7.157; coefficients of LDL-C, -3.999, -4.409, and -5.145; coefficients of HDL-C, -3.869, -4.555, and -5.215; and coefficients of TC, 3.984, 4.547, and 5.231, respectively. The adjusted coefficients of determination were 0.547, 0.593, and 0.678, respectively (P < 0.001, P < 0.001, and P < 0.001, respectively). Conclusion: Fasting TG levels can be calculated from TC, LDL-C, and HDL-C levels when nHDL-C levels are <160 mg/dL. Using nonfasting TG and eTG levels as indicators of hypertriglyceridemia might eliminate the need for venous sampling after overnight fasting.

Combination therapy with anamorelin and a myostatin inhibitor is advantageous for cancer cachexia in a mouse model.

Cancer cachexia is a multifactorial disease that causes continuous skeletal muscle wasting. Thereby, it seems to be a key determinant of cancer-related death. Although anamorelin, a ghrelin receptor agonist, has been approved in Japan for the treatment of cachexia, few medical treatments for cancer cachexia are currently available. Myostatin (MSTN)/growth differentiation factor 8, which belongs to the transforming growth factor-ß family, is a negative regulator of skeletal muscle mass, and inhibition of MSTN signaling is expected to be a therapeutic target for muscle-wasting diseases. Indeed, we have reported that peptide-2, an MSTN-inhibiting peptide from the MSTN prodomain, alleviates muscle wasting due to cancer cachexia. Herein, we evaluated the therapeutic benefit of myostatin inhibitory D-peptide-35 (MID-35), whose stability and activity were more improved than those of peptide-2 in cancer cachexia model mice. The biologic effects of MID-35 were better than those of peptide-2. Intramuscular administration of MID-35 effectively alleviated skeletal muscle atrophy in cachexia model mice, and the combination therapy of MID-35 with anamorelin increased food intake and maximized grip strength, resulting in longer survival. Our results suggest that this combination might be a novel therapeutic tool to suppress muscle wasting in cancer cachexia.